|Born||March 14, 1965
|Occupation||Actor, Film Producer|
|Years active||1973-1974, 1984, 1988-2001, 2005 – present|
|Spouse(s)||Kiran Rao (2005 – present)
Reena Dutta (1986 – 2002)
Aamir Hussain Khan (/ɑːmɪr xɑːn/; Hindi: आमिर ख़ान, Urdu: عامر حسین خان) (born March 14, 1965) in Mumbai, India, is a highly acclaimed and a prominent National Film Award-winning Indian film actor and producer.
Appearing as a child actor in Yaadon Ki Baaraat (1973), Khan’s career started eleven years later with the film, Holi (1984). He received his first commercial success with Qayamat Se Qayamat Tak (1988) and won a Filmfare Best Debut Award for his performance in the film. After eight previous nominations during the 1980s and 1990s, he received his first Filmfare Best Actor Award for his performance in Raja Hindustani (1996), his biggest commercial success so far. He won acclaim for his role in the Academy Award nominated Lagaan: Once Upon a Time in India (2001) and received his second Best Actor award at the Filmfare ceremony as well as numerous other awards. Taking a four year break from acting, Aamir made his comeback with Ketan Mehta’s The Rising (2005).
Being a part of several commercially successful movies and delivering highly acclaimed performances, he has established himself as one of the top and most successful leading actors of Hindi cinema.
Aamir was born in Mumbai into a Shia Muslim family that has been actively involved in the Indian film-industry. He is a descendant of Maulana Abul Kalam Azad and is originally from Shahbaad, Uttar Pradesh. His father Tahir Hussain is a producer; his uncle Nasir Hussain was a director. He has acted in a few films directed by his cousin Mansoor Khan. His brother Faisal Khan is an actor, and they have co-starred in the 2000 film Mela. His cousin Tariq was an actor in the 1970s who notably appeared in Yaadon Ki Baraat and Hum Kisi Se Kum Nahin.
Aamir began his career as a child actor in films like Yaadon Ki Baraat (1973) and Madhosh (1974). After eleven years, he made his acting debut in a supporting role with Ketan Mehta’s Holi (1984).
In 1988 he got his first leading role in Qayamat Se Qayamat Tak which was a huge success and launched his career. He went on to appear in many other films in the 1990s, which did poorly at the box office. However, Dil became the highest grossing films of 1990. Aamir went on to write the screenply for Mahesh Bhatt’s Hum Hain Rahi Pyaar Ke (1993), in which he also acted. Khan’s first and only release in 1996 was Dharmesh Darshan’s blockbuster Raja Hindustani opposite Karisma Kapoor. The film earned him his first Filmfare Best Actor Award after eight previous nominations during the 1980s and 1990s and went on to become one of the highest grossing films of its decade.
This was followed by the semi-hit Ishq (1997), which became the fourth highest grossing film of that year and the moderately successful Ghulam (1998), for which he did the playback singing. John Mathew Matthan’s moderately successful Sarfarosh (1999) was Khan’s first release in 1999. His role as a dedicated cop fighting border terrorism won him critical acclaim. His negative role in Deepa Mehta’s offbeat film Earth (1999) also won him acclaim.
In 2001 he produced and starred in the Academy Award nominated Lagaan: Once Upon a Time in India. The film became the third highest grossing film of that year and gave him his second Filmfare Best Actor Award. His second release, the moderately successful Dil Chahta Hai (2001) also entered into the top five highest grossing films of that year and earned him another nomination for Best Actor at the Filmfare ceremony.
For the next four years, Khan had no releases, as he put in a lot of time preparing for the role of the real-life martyr Mangal Pandey in his comeback film, The Rising (2005) Although the film was not as successful as Lagaan, it managed to do moderately well, becoming the third highest grossing film of that year.
Rakeysh Omprakash Mehra’s critically accliamed Rang De Basanti was Aamir’s first release in 2006. His role was well acclaimed, earning him a Filmfare Critics Award for Best Performance and various nominations for Best Actor including the Filmfare Awards. The film went on to become one of the highest grossing films of the year and was selected as India’s official entry to the Oscars Although the film was not shortlisted as a nominee, it won a nomination for Best Foreign Film at the BAFTA Awards in England. His performance in his next release, Fanaa (2006) was also acclaimed and the film went on to become one of the highest grossing films of 2006.
He fell in love with Reena Dutta (a Hindu). As Muslims, his parents did not approve of her. As soon as he turned 21, he proposed to her. She accepted and their marriage stayed a secret for a while.
Reena Dutta made a brief appearance in a song sequence in Khan’s first film, though not a professional actress and already married to him at that time. It was big news when the marriage was first revealed. Reena Dutta maintained a very low profile and continued her job working in a travel agency.
However, Aamir’s popularity survived the revelation, and his marriage to Reena seemed to have survived too. They had two children (son Junaid and daughter Aira) and led a quiet, publicity-shunning family life. Reena was even involved, briefly, in Aamir’s career when she worked as a producer for Lagaan. Then in December 2002, Aamir filed for divorce. Reena took custody of the children. On December 28, 2005, Aamir married again, to Kiran Rao, who had been an assistant to director Ashutosh Gowariker during the filming of Lagaan.
Awards and Nominations
|Yaadon Ki Baaraat||1973||Young Ratan|
|Qayamat Se Qayamat Tak||1988||Raj||Winner, Filmfare Best Debut Award
Nominated, Filmfare Best Actor Award
|Raakh||1989||Aamir Hussein||Nominated, Filmfare Best Actor Award|
|Love Love Love||1989||Amit|
|Tum Mere Ho||1990||Shiva|
|Dil||1990||Raja||Nominated, Filmfare Best Actor Award|
|Deewana Mujh Sa Nahin||1990||Ajay Sharma|
|Afsana Pyaar Ka||1991||Raj|
|Dil Hai Ki Manta Nahin||1991||Raghu Jetley||Nominated, Filmfare Best Actor Award|
|Isi Ka Naam Zindagi||1992||Chotu|
|Daulat Ki Jung||1991||Rajesh Chaudhry|
|Jo Jeeta Wohi Sikandar||1992||Sanjaylal Sharma||Nominated, Filmfare Best Actor Award|
|Parampara||1993||Ranbir Prithvi Singh|
|Hum Hain Rahi Pyaar Ke||1993||Rahul Malhotra||Nominated, Filmfare Best Actor Award|
|Andaz Apna Apna||1994||Amar||Nominated, Filmfare Best Actor Award|
|Baazi||1995||Inspector Amar Damjee|
|Aatank Hi Aatank||1995||Rohan|
|Akele Hum Akele Tum||1995||Rohit||Nominated, Filmfare Best Actor Award|
|Raja Hindustani||1996||Raja Hindustani||Winner, Filmfare Best Actor Award|
|Ghulam||1998||Siddharth Marathe||Nominated, Filmfare Best Actor Award
Nominated, Filmfare Best Male Playback Award
|Sarfarosh||1999||Ajay Singh Rathod||Nominated, Filmfare Best Actor Award|
|Mann||1999||Karan Dev Singh|
|Earth||1999||Dil Navaz||India’s official entry to the Oscars|
|Lagaan: Once Upon a Time in India||2001||Bhuvan||Winner, Filmfare Best Actor Award
Nominated for Academy Award for Best Foreign Language Film
|Dil Chahta Hai||2001||Akash Malhotra||Nominated, Filmfare Best Actor Award|
|The Rising||2005||Mangal Pandey||Nominated, Filmfare Best Actor Award|
|Rang De Basanti||2006||Daljeet (DJ)||Nominated, Filmfare Best Actor Award
Winner Filmfare Critics Award for Best Performance
India’s official entry to the Oscars
|Taare Zameen Pe||2007||Shahzad||Releasing December 21, 2007|
 Playback singing
|Akele Hum Akele Tum||1995||Aisa Zakhm Diya Hai||Voice over|
|Ghulam||1998||Aati Kya Khandala||Singer|
|Sarfarosh||1999||Is Deewane Ladke Ko||Singer|
|Mann||1999||Tumhare Bagair Jeena||Voice over|
|Mela||2000||Dekho 2000 Zamana Aa Gaya||Singer|
|The Rising||2005||Holi Re||Singer|
|Rang De Basanti||2006||Lalkaar||Voice over|
|Fanaa||2006||Mere Haath Mein||Voice over|
|Shah Rukh Khan
شاہ رخ خان
|Born||November 2, 1965
New Delhi, India
|Other name(s)||Shah Rukh Khan|
Shahrukh Khan (born November 2, 1965) (Hindi: शाहरुख़ ख़ान, Hindko: شاہ رخ خان) is a highly acclaimed Bollywood actor, producer, and recent host of the game show, Kaun Banega Crorepati.
Khan started out his career appearing in several television serials in the late 1980s. He made his film debut with the hit Deewana (1992) and has been part of numerous commercial successes as well delivering a variety of critically acclaimed performances. During his career years, he has won six Filmfare Best Actor Awards, and has had significant box office success, with films like Dilwale Dulhaniya Le Jayenge (1995) and Kuch Kuch Hota Hai (1998) being some of India’s biggest hits, while films like Kabhi Khushi Kabhie Gham (2001) Veer Zaara (2004) and Kabhi Alvida Na Kehna (2006) are the biggest Bollywood hits in the overseas market. Since then, Khan has established himself as one of the most prominent leading actors in Bollywood. Since 2000, he has branched out into film production and television presenting as well.
Shahrukh Khan was born to a Muslim family and raised by Hindus for most of his life. His father Taj Mohammed Khan was a freedom activist. His mother Lateef Fatima was the adopted daughter of Major General Shah Nawaz Khan of the Janjua Rajput clan , who served as a General in the Indian National Army of Subash Chandra Bose.
Khan’s father came to Delhi from the Kissa Kahani Bazaar in Peshawar now in Pakistan, before the Partition of India, while his mother’s family came from Rawalpindi, also in Pakistan. Khan has a sister named Shehnaz, who is lovingly known as Lalarukh. Khan attended St. Columba’s School where he was accomplished in sports, drama and academics. He won the Sword of Honour, an annual award bequeathed to the student who embodies most the spirit of the school. He later attended the Hansraj College (1985-1988) to earn an Honors degree in Economics.  After this, he studied for a Masters Degree in Mass Communications at Jamia Millia Islamia University..
After the death of his parents, Khan moved from New Delhi to Mumbai in 1991. In 1991, he married Gauri Khan in a Hindu wedding ceremony. They have two children, son Aryan (b. 1997) and daughter Suhana (b. 2000).
Nasreen Munni Kabir, the noted British filmmaker, produced a two-part documentary on Khan, titled The Inner and Outer World of Shah Rukh Khan (2005). Featuring his 2004 Temptations concert tour, the film contrasted Khan’s inner world of family and daily life with the outer world of his work. Another book Still Reading Khan was released in 2006 which details his family and his life. In 2007 another book by Anupama Chopra King of Bollywood “Shahrukh Khan” and the seductive world of indian cinema was released. This book described the world of Bollywood through Shahrukh’s life.
Khan’s life-size wax statue is available in Madame Tussauds wax museum., London, installed in April 2007 Khan has been chosen for the Ordre des Arts et des Lettres (Order of the Arts and Literature) award of the French government for his “exceptional career”.
 As Actor
Khan studied acting under celebrated Theatre Director Barry John, at Delhi’s Theatre Action Group (TAG). In 2007 John commented on his former pupil, “The credit for the phenomenally successful development and management of Shah Rukh’s career goes to the superstar himself.”  Khan started his acting career in 1988 appearing in the television series Fauji playing the role of Commando Abhimanya Rai. He went on to appear in several other television serials most notably appearing in the 1989 serial Circus, which depicted the life of circus performers and was directed by Aziz Mirza. That same year he also had a minor role in the English language made-for-television film In Which Annie Gives it Those Ones, which was written by Arundhati Roy and based on life at Delhi University.
After the death of his parents Khan moved from New Delhi to Mumbai in 1991.  He made his Bollywood film debut in Deewana (1992) which was a box office hit and launched his career in Bollywood. His debut performance won him a Filmfare Best Debut Award. His second release Maya Memsaab was known for its controversial issues as Khan appeared in what was apparently an “Explicit for Bollywood” sex scene for the film. .
In 1993 he won acclaim for his performances as a murderer and obsessive lover respectively in the box office hits Baazigar and Darr. He won his first Filmfare Best Actor Award for his performance in Baazigar. He was also appreciated for his role as a young loser in Kundan Shah’s Kabhi Haan Kabhi Naa which earned him the Filmfare Best Actor Award (critics) that same year. In 1994 Khan once again played an obsessive lover/psycho role in Anjaam. Even though the movie wasn’t a box office success Khan’s performance in a negative role earned him the Filmfare Best Villain Award.
In 1995 he starred in Aditya Chopra’s directorial debut Dilwale Dulhania Le Jayenge which was a critical and commercial success and has entered its twelfth year in Mumbai theaters, grossing over 12 billion rupees in all, making it as one of the biggest film blockbusters. 
1996 was a disappointing year for Khan as all his films released that year flopped.. 1997 meant his diminutive comeback, as his first release, Yash Chopra’s Dil to Pagal Hai went on to be the year’s second highest grossing film. . That same year he also had success with Subhash Ghai’s Pardes which was one of the biggest hits of the year and Aziz Mirza’s moderately successful film Yes Boss.
Khan was welcomed with similar success in 1998 starring in Karan Johar’s directional debut Kuch Kuch Hota Hai which was the biggest hit of the year and won him his fourth Best Actor award at the Filmfare. He also won critical praise for his performance in Mani Ratnam’s Dil Se which did not do well at the box office in India, but earned good collections overseas. 
1999 was another non-notable year for Khan with the average hit Baadshah as his only film release that year. The year 2000 saw good success, with Aditya Chopra’s second directional film Mohabbatein doing well at the box office, and Mansoor Khan’s hit Josh. He gained critical acclaim for his performance in the former, which won him his second award for Best Actor (critics) at the Filmfare. In that same year, Khan set up his own production house Dreamz Unlimited with Juhi Chawla. Both Khan and Chawla starred in the first film from their production house Phir Bhi Dil Hai Hindustani. He also played a supporting role in Kamal Hassan’s controversial film Hey Ram for which he recieved much acclaim although the film was a failure at the box office..
In 2001, Khan collaborated with Karan Johar for the second time with the multi-starrer family drama film Kabhi Khushi Kabhie Gham, which was one of the biggest hits of the year. He also received favorable reviews for his performance as Emperor Asoka in the historical epic Asoka.
In 2002, Khan played the title role in Sanjay Leela Bhansali’s award-winning period romance Devdas which was the third Hindi adaptation of Sharat Chandra Chattopadhyay’s famous novel of the same name after the 1936 version Devdas and the 1955 version Devdas.
In 2003, Khan starred in the romantic drama Chalte Chalte which was a semi-hit.. He then made his third film with Karan Johar as the writer and Nikhil Advani as a director of the romantic tearjerker Kal Ho Naa Ho. The movie was one of the year’s biggest hits in India and in the overseas market as well. Khan’s performance in this film as a guy who has heart disease was also well received.
2004 proved to be a good year for Khan commercially and critically as well. He starred in Main Hoon Na which was the directorial debut of choreographer Farah Khan. The movie did well at the box office, whilst Yash Chopra’s Veer-Zaara was the biggest hit of that year. Khan’s performance in the latter was much appreciated and he won various awards at several award ceremonies. Khan also won critical praise for his performance in Ashutosh Gowariker’s Swades, which won him the Filmfare Best Actor Award for the sixth time although the film was a box office failure..
His only major film release in 2005 was the fantasy film Paheli which was not as successful at the box office, but won him acclaim. .
In 2006 he once again collaborated with Karan Johar for the multi-starrer melodrama film Kabhi Alvida Na Kehna which did well in India and became the biggest hit in the overseas market.. That same year he played the title role in Don, a remake of the 1978 hit film Don which was also successful 
His most recent film was the sports film Chak De India which released on August 10, 2007. Khan received good reviews for his performance as the coach of a girl’s hockey team in the film and the film is doing well at the box office despite a slow start./ He recently made a cameo appearance in Farah Khan’s brother Sajid Khan’s directorial debut Heyy Babyy which released on August 24, 2007. His other forthcoming release is Om Shanti Om.
 As a Producer
Khan has also produced some of the films he has starred in but has had mixed success as both the producer and the star of his films. He set up a production company called Dreamz Unlimited with Juhi Chawla and director Aziz Mirza in 1999. The first two of the films he produced and starred in: Phir Bhi Dil Hai Hindustani (2000) and Asoka (2001) were box office failures.. His third film, as a producer and star, Chalte Chalte (2003), was the first box office hit from his production house.. In 2004 he set up another production company called Red Chillies Entertainment and produced and starred in Main Hoon Na which was another hit at the box office.. In 2005 he produced and starred in the fantasy film Paheli, which was India’s selection for the Academy Awards (foreign films category) but did not win. At the box office Paheli was a disappointment. That same year he also co-produced the supernatural horror film Kaal with Karan Johar and performed an item number for the film with Malaika Arora Khan. Kaal was moderately successful at the box office.
The forthcoming film produced by his company Red Chillies Entertainment is Om Shanti Om which he will also star in.
 As Television Host
Khan was chosen as the host of the third series of the popular game show Kaun Banega Crorepati, the Indian version of Who wants to be a millionaire?, in 2007 taking over from the original host Amitabh Bachchan who had hosted the show from 2000 to 2005. The show is deemed the most popular programme in Indian television history. On Monday, January 22, 2007, “KBC” aired with Khan as the new host. The season ended on April 19 2007.
Awards and nominations
|1992||Deewana||Raja Sahai||Winner, Filmfare Best Debut Award|
|Raju Ban Gaya Gentleman||Raju (Raj Mathur)|
|Dil Aashna Hai||Karan|
|Baazigar||Ajay Sharma/Vicky Malhotra||Winner, Filmfare Best Actor Award|
|Darr||Rahul Mehra||Nominated, Filmfare Best Villain Award|
|1994||Kabhi Haan Kabhi Naa||Sunil||Winner, Filmfare Critics Award for Best Performance|
|Anjaam||Vijay Agnihotri||Winner, Filmfare Best Villain Award|
|1995||Karan Arjun||Arjun Singh/Vijay|
|Zamana Deewana||Rahul Malhotra|
|Oh Darling! Yeh Hai India||Hero|
|Dilwale Dulhania Le Jayenge||Raj Malhotra||Winner, Filmfare Best Actor Award|
|Ram Jaane||Ram Jaane|
|1996||English Babu Desi Mem||Vikram/Hari/Gopal Mayur|
|Dushman Duniya Ka||Badru|
|Yes Boss||Rahul Joshi||Nominated, Filmfare Best Actor Award|
|Dil To Pagal Hai||Rahul||Winner, Filmfare Best Actor Award|
|1998||Duplicate||Bablu Chaudhry/Manu Dada||Nominated, Filmfare Best Villain Award|
|Dil Se||Amarkant Varma|
|Kuch Kuch Hota Hai||Rahul Khanna||Winner, Filmfare Best Actor Award|
|1999||Baadshah||Raj ‘Baadshah’Heera||Nominated, Filmfare Best Comedian Award|
|2000||Phir Bhi Dil Hai Hindustani||Ajay Bakshi|
|Hey Ram||Amjad Ali Khan||Tamil film. India’s official entry to the Oscars|
|Har Dil Jo Pyar Karega||Rahul||Special appearance|
|Mohabbatein||Raj Aryan Malhotra||Winner, Filmfare Critics Award for Best Performance
Nominated, Filmfare Best Actor Award
|Gaja Gamini||Shahrukh||Special appearance|
|2001||One 2 Ka 4||Arun Verma|
|Kabhi Khushi Kabhie Gham||Rahul Raichand||Nominated, Filmfare Best Actor Award|
|2002||Hum Tumhare Hain Sanam||Gopal|
|Devdas||Devdas Mukherjee||Winner, Filmfare Best Actor Award
India’s official entry to the Oscars
|Shakti: The Power||Jaisingh||Special appearance|
|Saathiya||Yeshwant Rao||Special appearance|
|2003||Chalte Chalte||Raj Mathur|
|Kal Ho Naa Ho||Aman Mathur||Nominated, Filmfare Best Actor Award|
|2004||Yeh Lamhe Judaai Ke||Dushant|
|Main Hoon Na||Maj. Ram Prasad Sharma||Nominated, Filmfare Best Actor Award|
|Veer-Zaara||Veer Pratap Singh||Nominated, Filmfare Best Actor Award|
|Swades||Mohan Bhargava||Winner, Filmfare Best Actor Award|
|2005||Kuch Meetha Ho Jaaye||Himself||Special appearance|
|Kaal||Special appearance in song Kaal Dhamaal|
|Paheli||Kishen/The Ghost||India’s official entry to the Oscars|
|The Inner and Outer World of Shah Rukh Khan||Himself (Biopic)||Documentary directed by British-based author and director Nasreen Munni Kabir|
|2006||Alag||Special appearance in song Sabse Alag|
|Kabhi Alvida Naa Kehna||Dev Saran||Nominated, Filmfare Best Actor Award|
|Don – The Chase Begins Again||Don/Vijay||Nominated, Filmfare Best Actor Award|
|I See You||Special appearance in song Subah Subah|
|2007||Chak De India||Kabir Khan|
|Heyy Babyy||Special appearance in song Mast Kalandar|
|Om Shanti Om||Om||Releasing on November 9, 2007|
|Dulha Mil Gaya||Raj||Releasing on November 23, 2007|
- Phir Bhi Dil Hai Hindustani (2000)
- Asoka (2001)
- Chalte Chalte (2003)
- Main Hoon Na (2004)
- Kaal (2005)
- Paheli (2005)
- My Name Is Anthony Gonsalves (2007)
- Om Shanti Om (2007)
- Apun Bola – Josh (2000)
- Khaike Paan Banaraswala – Don- The Chase Begins Again (2006)
- Ek Hockey Doongi Rakh Ke–Chak De India (2007)
- Kuch Kuch Hota Hai (1998)
- Main Hoon Na (2004)
- Kabhi Alvida Naa Kehna (2006)
- Chak De India (2007)
- Fauji (1988) … Abhimanyu Rai
- Dil Dariya (1988)
- Circus (1989)
- In Which Annie Gives It Those Ones (1989)
- Idiot (1991) … Pawan Raghujan
- Kareena Kareena (2004) Zee TV … Special Appearance
- Kaun Banega Crorepati (2007) … Host
|Born||January 10, 1974
Mumbai, Maharashtra, India
|Spouse(s)||Sussanne Roshan (December 2000 – present)|
Hrithik Roshan (Hindi: ऋतिक रोशन, Urdu: رتک روشن, pronunciation: /rɪt̪ɪk roːʃən/ / born 10 January 1974), nicknamed Duggu, is a highly acclaimed Bollywood actor and five time Filmfare Award winner.
Roshan, who began his career as a child actor, made his film debut as a leading actor with the blockbuster Kaho Naa Pyaar Hai (2000), which earned him two awards for Best Actor and Best Debut at the Filmfare ceremony, as well as numerous other awards. During his career years, he was praised for his performances in films like Koi Mil Gaya (2003), Krrish (2006) and Dhoom 2 (2006), being his biggest commercial successes so far, and winning him many Best Actor awards each. This way he has established himself as one of the most prominent leading actors of India.
Roshan’s first movie role was as a child artist when he was six years old in the 1980 movie Aasha, where he appeared in a dance sequence as an extra. Roshan went on to play minor roles in Aap Ki Deewane (1980) and Bhagwan Dada (1986) both of which were produced by and starred his father in the leading role. He then became an assistant director assisting in the production of his father’s films such as Karan Arjun (1995) and Koyla (1997).
Roshan made his debut as a leading man in the 2000 film Kaho Naa… Pyaar Hai opposite another debutante actress Amisha Patel. The film was directed by his father and proved to be very successful at the box office, becoming the highest grossing film of 2000 and winner of the Filmfare Best Movie Award. Roshan’s performance earned him the Filmfare Best Debut Award and the Filmfare Best Actor Award. The film Kaho Naa… Pyaar Hai entered the Limca Book of Records in 2003 for the most number of Awards won by a Bollywood Film – 102 awards.
In 2000, Roshan starred in Fiza, which did poorly commercially but was critically acclaimed, and the moderately successful Mission Kashmir which was the third highest grossing film of the year.
In 2001, Hrithik starred in Yaadein which was a failure at the box office and Kabhi Khushi Kabhie Gham which did extremely well at the box office, becoming the second-highest grossing film of 2001.
Roshan had an unsuccessful year in 2002 when all three of his releases – Mujhse Dosti Karoge!, Na Tum Jaano Na Hum, Aap Mujhe Achche Lagne Lage – failed to make an impact the box office and were declared flops. In 2003, he made a comeback with the science-fiction film Koi… Mil Gaya which was the highest grosser of the year and also won many Filmfare Awards, including another Filmfare Best Actor Award and the first Filmfare Best Actor (Critics) for Hrithik. He had only one release in 2004, Lakshya, directed by Farhan Akhtar, which did not do well at the box office although critics called it his most impressive performance so far.
Roshan took a two-year break from acting before resurfacing with the superhero film Krrish, a sequel to his 2003 hit Koi Mil Gaya which released in June 2006. Krrish was a major box office success and one of the highest grossers of 2006. His most recent release of 2006 is Dhoom 2, a sequel to the 2004 hit Dhoom, in which he played a negative role (a villain) for the first time. The film went on to become the highest grossing film of 2006, as well as one of the most successful films of Bollywood. Both Krrish and Dhoom 2 won him acclaim. He won his third Filmfare Best Actor Award for his performance in Dhoom 2 as well as numerous other Best Actor awards for his performance in Krrish.
Hrithik Roshan was born in Mumbai, India, to Pinky and actor/director Rakesh Roshan. He is the nephew of well-known music director Rajesh Roshan. Music director Roshan is Hrithik’s paternal grandfather, and veteran producer and director J. Om Prakash his maternal grandfather. Hrithik has a supernumerary thumb on his right hand.
Roshan is married to Sussanne Khan (who is now Sussanne Roshan), his high-school sweetheart and daughter of Sanjay Khan. Film clans (see List of Bollywood film clans) tend to intermarry.
The couple had their first child, a baby boy, on March 28, 2006 at Lilavati Hospital in Mumbai, India. The child was named Hrehaan.
In 2001, a rumour alleging Roshan made disparaging remarks about Nepal and its people caused outrage in the country. Several newspapers carried the report, leading to student protests, in which four people died. The unrest the protests caused forced the government to cancel a flight from Kathmandu to India. Later the Indian embassy and the actor himself clarified that he had made no such remarks.
In 2006, at the London press conference for his film Krrish, Roshan said that he knew it was time to leave Shanghai and Hong Kong after six weeks of stunt training and go home when his eyes started “turning into little slits like the Chinese”.
Koi Mil Gaya (2002)
Main Prem Ki Deewani Hoon (2002)
Mujhse Dosti Karoge (2002)
Na Tum Jaano Na Hum (2002)
Aap Mujhe Achche Lagne Lage (2001)
Kabhi Khushi Kabhie Gham (2001)
Mission Kashmir (2000) …. Altaaf
Fiza (2000) …. Amaan Ikramullah
Kaho Naa Pyaar Hai (2000) …. Rohit/Raj
Bhagwan Dada (1986)
Aap Ke Deewane (1980)
Smoking and Breast Cancer.
Cigarettes may cause more cases than the two so-called breast cancer genes combined.
By now, most people have heard the grim statistic of breast cancer: almost one in every eight women in the U.S. will develop the disease in her lifetime. This year alone, breast cancer will take the lives of roughly 45,000 American women.For most women, the top risk factors for breast cancer are hormonal,such as start-ing menstruation at a young age (before 12 years
old), going through menopause late in life (after age 50), having few or no children and having a
first full-term pregnancy at a late age. All these traits share one common feature: they contribute to a longer lifetime exposure to estrogen, which can spur the growth of breast cells into cancerous tumors. Estrogen levels rise at the onset of menstruation and decrease at menopause. Increasing physical activity and eating a diet rich in fruit and vegetables may decrease risk. Family history also is an important risk factor for breast cancer. Because breast cancer is fairly common, many women have one or two relatives with breast cancer by chance.
But some young women whose mother, grandmothers or sisters had breast (or ovarian) cancer
carry an inherited susceptibility for the disease. Women from such high-risk families frequently
carry mutations in the BRCA1 or BRCA2 gene. Mutations in these genes confer between a 40
and 90 percent lifetime risk of developing breast cancer. Although these familial cancer syndromes are devastating, they account for only about 5 percent of all breast cancer cases. The other 95 percent—the nonfamilial, or sporadic, breast cancers—are caused, in part, by the hormonal risk factors mentioned above and by some risk factors we are only now beginning to explore. We believe that one important and preventable risk factor for breast cancer is cigarette smoking. Our research suggests that roughly half of all women are particularly sensitive to the carcinogens found in tobacco and so have a higher risk of breast cancer if they smoke cigarettes. Such women have a slow-acting form of a liver enzyme that normally detoxifies carcinogens. Because these women’s “detox” enzymes act more slowly than the enzymes of other women, the carcinogens in tobacco last longer in their bodies, allowing the substances more time to cause cancer. For such women, every cigarette loads the dice in favor of breast cancer.
Epidemiologists have been intrigued for years by hints that smoking can cause breast cancer. But for every study that purports to show a link between smoking and breast cancer, others fail to demonstrate any association—and some even show that cigarette smoking decreases a woman’s risk of breast cancer. This is surprising because smoking causes so many other cancers, such as lung and bladder cancer. The reason for the discrepancy might be related to a complicated interaction among unidentified chemicals present in cigarette smoke that might lower estrogen levels in the blood of some women, thereby lowering their risk of breast cancer. Smoking also appears to lower the age at which a woman goes through menopause, which would also lower breast cancer risk because estrogen levels drop at menopause. Although many previous studies do not impliby.
Heart Disease and Stroke.
The American Heart Association’s recent survey suggests that only 8 percent of American women recognize that heart attack and stroke are their greatest health threats. Why do women fail to appreciate the risk these diseases pose to them?
I think it’s primarily a lack of awareness of what the facts are. They haven’t heard it on the news, and they haven’t heard it from their physicians. Most women are shocked when they
hear that although one out of eight women die of breast cancer, one out of two die of heart disease or stroke. In other words, half of all American women will die of heart disease or stroke.
And yet when we asked American women to name their greatest health threat, 61 percent said cancer, particularly breast cancer. Breast cancer is a very serious threat—we don’t underestimate that at all. But we think that women should also be aware of their risk of heart disease and stroke—and know how to protect themselves.
Do women’s symptoms of heart disease differ from men’s?
Research shows that chest pain remains the most common manifestation of coronary artery disease in both men and women. Like men, women experience angina, the chest pain that occurs when the heart’s blood supply is inadequate. But women are more likely than men to have other symptoms that are more subtle, such as nausea, abdominal pain or fatigue. Sometimes we see a woman who has the classic chest pain, but when we probe we find that she’s been having these
other symptoms for a week or two but didn’t recognize them as symptoms of heart disease or that her physician didn’t recognize them as such.
Previous research has shown that physicians historically have been less likely to order diagnostic tests— such as electrocardiogram (ECG) stress testing—to detect heart disease in their female patients than in their male patients. Is this still true today?
It is somewhat true, but it is not the only explanation for the lack of predictive diagnostic testing for heart disease in women. Women usually have more advanced heart disease—and at older
ages—than men, probably because estrogen protects women from developing coronary artery disease until after menopause. But because they’re older, women tend to suffer more from complicating conditions, such as diabetes. All of that poses challenges to diagnosing women accurately. And, of course, until recently women weren’t included in very many clinical trials. So for a long time physicians really didn’t recognize heart disease as a problem for women. But now there’s an increase in awareness. An enormous amount of energy and effort is going into educating physicians and other health care providers—as well as women themselves.
What You Can Do
Are there things women can do to ensure that they are diagnosed and treated effectively for heart disease and stroke?
Yes. One thing women can do is to begin to evaluate their own risk factors. Have you had your cholesterol measured? Do you know what your numbers mean? The American Heart Association has set up a free hotline, 888-MY-HEART, for women to call for information on coronary artery disease and stroke. The AHA has also developed a risk-assessment guide so that women can evaluate their own personal risk factors for heart disease .Women need to take charge about knowing what their risk factors are and what they should be doing to protect their own health. Get all the information you can. In some cases, you have to become very assertive. You have to walk into the doctor’s office and say, “Hello, how are you, I’ve got some questions.” Don’t wait until you’re walking out the door, and the doctor’s already got his or her mind on the next patient. Bring your agenda forward early in the visit.
How do the female sex hormones, estrogen and
progesterone, protect women from heart disease?
We know that they help lower LDL cholesterol, the bad cholesterol, and that they help to raise HDL cholesterol, the good cholesterol. They also appear to help dilate blood vessels. Bigger
coronary arteries are less likely to trigger a heart attack. And it appears that estrogen and progesterone have an antioxidant effect on LDLs. Researchers believe that oxidized
LDLs help kick off the process of atherosclerosis. So antioxidants may help by countering that artery-clogging tendency. Many studies are now looking at these issues; I think we will
know a lot more soon.
Do women have different risk factors for heart disease than men?
The only gender-specific risk factor that women face is the loss of estrogen that they normally experience with aging. It is quite controversial whether menopause itself increases a woman’s
risk of heart disease. Women start losing estrogen well before menopause. In fact, you see a drop in estrogen in women in their 40s. Perimenopause—the period around menopause—
can add up to a decade or more. So estrogen levels drop earlier than the narrow point in time of menopause, when a woman experiences her last menstrual period. When should women start thinking about heart disease and stroke? Don’t wait until you haven’t had a period for two years. It’s never too early to start asking what you can do to prevent, delay or minimize your risk of heart disease. As for stroke, women should start thinking about their risk fairly early in life. A third of the strokes occur before the age of 60. And they are devastating. When a 30-year-old woman has a stroke, it’s a tragedy because it was preventable. An Ounce of Prevention
What does research reveal about how to prevent heart disease in women?
Tobacco is the number-one issue. There’s been a steady rise in the number of female smokers, and there’s a lot of evidence to suggest that many women use tobacco for weight control— not just to be “cool.” The weight issue makes it harder to convince females to quit. What they’re concerned about is weight gain as they quit. So an important issue for women who are going to quit smoking is exercise. They should make plans to increase their physical activity because they might eat more. Not smoking is the single most important thing you can do to reduce your risk of heart disease. If you already smoke, quit. The second most important thing is to know your total cholesterol level and blood pressure. If they are elevated, then initiate lifestyle modifications, such as controlling your weight. You can do that by changing both your eating patterns and your amount of physical activity. The third thing you can do is to look at your alcohol intake, which can elevate both blood pressure and triglycerides, fats in the blood that can pose a particular risk of heart disease for women. So moderate or reduce— or, if necessary, eliminate—alcohol consumption.
Doesn’t current research indicate that a drink a day can reduce the risk of heart disease?
Moderate alcohol intake has been associated with lower rates of coronary artery disease. But if you’re taking in a lot of empty calories as alcohol, it becomes a problem for weight control. The other issue is there is a relation that is not clearly understood between alcohol and high blood pressure. So women who have high triglycerides and hypertension and are struggling with their weight need to be cautious about drinking.
How can women reduce their risk of stroke?
Number one: they should stop smoking. Number two: women need to look at alternative forms of birth control besides the pill. Number three: women should take steps to reduce their blood
pressure and their risk of heart disease. People who suffer from heart disease also have a greater risk of suffering a stroke.
Is it ever too late to reduce our risk of heart attacks and stroke?
Not really. Even in nursing homes, among people who have been very, very sedentary, it has been shown that walking reduces weight. That, in turn, can help reduce blood pressure and improve the cholesterol profile, lowering the risk of heart attack and stroke.
Hormone replacement therapy is known to protect postmenopausal women from heart disease. Yet it can also pose other potential problems, including an increased risk of breast cancer. What’s a woman to do?
The question of whether to use hormone replacement therapy has to be an individual decision. A woman really needs to sit down and talk with her physician about her own situation. What stage of menopause is she in? What symptoms is she experiencing? What’s her family history of heart disease and cancer? And what about osteoporosis? There’s very strong evidence concerning the benefits of hormone replacement therapy for preventing osteoporosis. In my family, for example, all the women get osteoporosis. Frankly, that motivates me to take hormone replacement therapy even more than the potential cardiovascular benefits, because I’ve seen how painful and debilitating osteoporosis can be. And as new hormone replacement therapies come out, they’ll have fewer adverse effects. For many women, that’s going to be very important. Because the data show that about a third of women who have a prescription for hormone replacement therapy never fill it, in part because they’re afraid of side effects
or breast cancer. Another third start taking it but then stop within two to three months because they gain weight, develop painful, swollen breasts or experience some other side effect. That tells us that each woman has to be involved in the decision-making process in order to be committed.
How important is obesity as a risk factor for heart disease in women?
The obesity issue is getting quite interesting. More studies are being done in different populations, using different methodologies. Some of the results are contradictory. One study may say obesity is a big risk factor. Other studies say people can gain weight, and as long as they are fortunate enough not to develop high blood pressure, high blood cholesterol or diabetes,
it isn’t so bad. I believe that obesity by itself can pose a problem: it increases the burden on the heart.
What lies ahead?
This is a very exciting time. There’s a lot of research on women and heart disease being conducted right now, and there are numerous opportunities for women to participate in research. Women who have an interest might want to call their local academic health center to find out what kinds of studies are going on in their area. There’s an old saying: “You see what you look for, and you look for what you know.” Now that we know that heart disease is a major
health problem for women, more people are looking for it, and they’re seeing it. And that means
that more women are being treated earlier in the course of the disease and that many more are
learning how they can prevent heart disease and stroke.
What Do the Cholesterol Numbers Mean?
The most common cholesterol test is for total cholesterol, measured in milligrams per deciliter of
blood (mg/dL). But it’s also important to know your HDL level—the amount of high-density lipoprotein, or good cholesterol, in your blood. The American Heart Association (AHA) says healthy women should have less than 200 mg/dL total cholesterol and at least 35 mg/dL of HDL cholesterol. Total cholesterol levels between 200 and 239 mg/dL are considered borderline-high, and those greater than 240 mg/dL are considered high. If your HDL cholesterol levels are too low, you should also have your low-density lipoprotein (LDL), or bad cholesterol, checked—it should be lower than 130 mg/dL. Some physicians prefer to analyze your cholesterol ratio: your total cholesterol divided by your HDL cholesterol. The optimal ratio for women is 3.5 to 1; anything above 5 to 1 is a health risk.
What’s in Store for the Future
By the turn of the century, approximately 50 million women in the U.S. will be age 50 or older. Inevitably, that will translate into more women with heart attacks, strokes and other cardiovascular diseases. Unfortunately, most of the scientific knowledge about these disorders has been based on studies of middle-aged men. That gender gap will soon narrow. Researchers have launched several studies of cardiovascular disease in women that should yield results in the
coming decade. By the time female baby boomers enter the cardiovascular risk zone after menopause, researchers should have a better understanding of the female heart and circulatory
system. Here are some of the top questions about women, heart disease and stroke—and how researchers plan to answer them. Does estrogen really protect against heart disease? Although many studies have shown a lower rate of heart attacks among women taking estrogen as part of hormone replacement therapy, no single investigation has been large enough or has lasted long
enough to prove estrogen’s benefits definitively—or to show beyond a doubt that estrogen’s heart-healthy effects outweigh its risks for breast cancer. In 1991 the National Institutes of Health launched a massive clinical trial called the Women’s Health Initiative, which will see if estrogen replacement therapy will reduce the risk of heart attack in postmenopausal women. Part of the study will involve more than 25,000 postmenopausal women across the country:
some will take estrogen or a combination of estrogen and progestin called hormone replacement
therapy; others will take an inactive placebo pill. Epidemiologist Elizabeth L. Barrett-Connor of the University of California at San Diego predicts that the Women’s Health Initiative should answer the estrogen question in five to 10 years. In the meantime, a report published in the New England Journal of Medicine last December suggests that an estrogenlike drug named raloxifene lowers women’s blood concentrations of low-density lipoprotein (LDL), the bad cholesterol that when elevated leads to atherosclerosis and an increased risk of a heart attack. Raloxifene is one of the new selective estrogen receptor modulators (SERMs), which promise the benefits of estrogen without its cancer risk. How might estrogen work to protect against
heart disease? If estrogen is confirmed to prevent heart disease, the next question will be how it does so. A preliminary study presented at an American Heart Association conference in March
suggests that estrogen shields premenopausal women from heart disease by lowering their blood levels of an enzyme called hepatic lipase. John E. Hokanson of the University of Washington reported at the conference that the hepatic lipase levels of 25 men were 53 percent higher than those of 39 premenopausal women. Hepatic lipase is known to help form the worst type of LDL—the so-called small, dense LDL—which is most likely to clog arteries. Hokanson notes that estrogen appears to regulate the activity of hepatic lipase. Researchers are now examining whether postmenopausal women, who have lowered estrogen levels, have higher levels of hepatic lipase than premenopausal women. Should women take aspirin to prevent a heart attack? Many doctors now tell their healthy male patients to take a low dose of aspirin regularly, based on a report in 1988 by epidemiologist Charles H. Hennekens of Harvard Medical School and his colleagues. The study showed that middleaged men who took an aspirin every other day cut their risk of suffering a first heart attack dramatically. In 1991 the same
researchers published results from the Nurses’ Health Study hinting that aspirin’s benefits might also transfer to women. After tracking the health of the more than 80,000 women in the Nurses’ Health Study for six years, the researchers found that women age 50 and older who took an aspirin between one and six times a week had one-third fewer heart attacks than women who didn’t. Hennekens and his colleagues are now conducting a study to evaluate the risks and benefits of low-dose aspirin versus a placebo among another group of 40,000 female doctors, nurses and other health professionals. Within the next several years, Hennekens says,
the new Women’s Health Study should indicate whether women would be wise to pop an aspirin every other day along with their male partners. Do vitamins prevent heart disease in women? No wonder women are confused. In 1993 the Nurses’ Health Study showed that women who took vitamin E supplements regularly had a lower risk of heart disease than women who didn’t. But three years later a study by Lawrence H. Kushi of the University of Minnesota School of Public Health indicated that women can get the heart benefits of vitamin E only by eating a diet rich in the nutrient—not by taking dietary supplements. The Women’s Health Study should clear up the confusion over vitamin E within three to four years. It should also confirm the heart benefits of vitamins B6 and folate, which the Nurses’ Health Study earlier this year suggested might also reduce women’s risks for heart disease. But even once the results on B6 and folate are in, Hennekens advises that it is most important for women to focus on reducing their known
risk factors for heart disease. Why are African-American women at greater risk of dying from cardiovascular disease than Caucasian women? Black women with cardiovascular disease are 69 percent more likely to die than their white counterparts, according to the American Heart Association. To account for this racial disparity, Lori J. Mosca—a preventive cardiologist at the University of Michigan and a member of the American Heart Association’s task force on women and cardiovascular disease— and her colleagues are now analyzing health data gathered over the past 40 years on 30,000 white and black women. Mosca speculates that black women are more likely to die than white women because they tend to have more cardiovascular risk factors, such as high blood pressure. Left untreated, high blood pressure can result in more severe heart disease and a greater risk of death, she says. Mosca and her team expect preliminary results by 2000.
Success of dieting.
Given the limited success of dieting—and the risks—is it better just to stay plump?
I couldn’t believe my eyes. But there it was, printed in an editorial entitled “Losing Weight—An Ill-Fated New Year’s Resolution” in the January 1 New England Journal of Medicine: “Unfortunately, the data…showing the beneficial effects of weight loss are limited, fragmentary and often ambiguous.” For someone like me who has struggled with her weight for years, this dry pronouncement from the medical profession’s equivalent of the Voice on High was nothing short of a revelation. As a chubby child, a “baby-fat” teenager and a Rubenesque woman, nearly all my visits to doctors have inevitably ended with some version of the statement, “If you could lose 10/20/30 pounds, you would sleep better/have more energy/ have lower blood pressure/(fill in blank here).” Lose weight? In theory, it’s no problem. I’m an expert at counting calories, calculating fat grams and figuring out just how much time on the StairMaster absolves the sin of eating an Oreo. I’m a veteran of the Grapefruit Diet, Weight Watchers and Diet Center, and I even survived the deadly liquid-protein diets of the 1970s. I took my first diet drug—one of Mother’s prescription tablets cut in half—at age 10. I calculate that since the age
of 18, I’ve lost (and gained and lost again) a total of at least 120 pounds—and at 5¢6² I’ve never weighed more than 196. The pitfall to losing weight, as every serious dieter knows, is that what comes off doesn’t usually stay off. A group of experts convened in 1992 by the National Institutes of Health concluded that at least 90 percent of dieters put the pounds right back on within five years. And losing weight and keeping if off becomes harder and harder as we get older; even thin people tend to gain between 10 and 20 pounds between their 20s and 60s.
So I found myself cheering inwardly when I read the New England Journal editorial. Could this mean that it’s okay— healthwise, if not socially—to be fat? Should people like me call a truce in their battles with their bodies and just get on with life? Or would we just be deluding ourselves?
A Widening Problem?
There are a lot of us. Indeed, a startling percentage of women in the U.S. fall into the category “obese,” including some who might be startled because they probably consider themselves
simply plump. The National Center for Health Statistics says that more than one third of all American women are overweight, including nearly half of those between the ages of 55 and 64. The market for women’s plus sizes (sizes 16 and up) is a booming $22.7 billion a year. African-American and Latin-American women are even more likely than Caucasian women to be obese: the Second National Health and Nutrition Examination Survey found that 44 percent of black women and 35 to 40 percent of Hispanic- American women are overweight, compared with 25 percent of white women. Although socioeconomic factors and cultural differences in diet undoubtedly play a role in the racial breakdown of obesity, most obesity researchers believe genetics is also important. (That is, after all, why they study the genetics of mouse strains with names like Obese and Tubby.) In a telling study reported earlier this year, Claude Bouchard of the University of Laval in Quebec and his colleagues found that both members of 12 pairs of adult male twins who ate 1,000 extra calories a day for 100 days gained the same amount of weight. But the exact amount of weight the men gained varied up to sixfold between sets of twins. Such indications that human obesity has a genetic underpinning don’t shock me: both my grandmothers and most of my great-aunts tipped the scales at 250 plus, even though the tallest was 5¢5². (Of course, it could have been the family recipe for that time-honored Southern dish, pecan pie.)
The Risks of Being Fat
Despite the fact that obesity is so prevalent, sound medical advice is hard to come by. It’s tough to know whom to believe. When launching the nonprofit organization Shape Up America! in 1994, former Surgeon General C. Everett Koop said obesity
causes 300,000 deaths in the U.S. every year, second only to smoking. But in their January editorial, the New England Journal’s top editors, Jerome P. Kassirer and Marcia Angell, called
the 300,000 figure “by no means well established” and wrote that it is “derived from weak or incomplete data.” So what are healthy figures—both in terms of statistics and body weight? Prompting the editorial was a report published in the same issue of the journal by June Stevens of the University of North Carolina at Chapel Hill and her colleagues. Stevens and her co-workers reported the results of analyzing health data gathered from 262,019 female and 62,116 male nonsmokers during the American Cancer Society’s Cancer Prevention Study I, which was conducted between 1960 and 1972. The researchers found that excess body weight slightly increases the risk of death from any cause among people between 30 and 74
years of age. The Stevens report was by no means an unusual finding: in 1995 the New England Journal published a study linking body weight and mortality in 115,195 women between 30 and 55 years old who were part of the massive, ongoing Nurses’ Health Study. And last year the Journal of the American Medical Association (JAMA) weighed in with two reports on the health hazards of obesity in women. In a separate report in JAMA on data from the Nurses’ Health
Study, a group from Harvard Medical School found that women who put on weight as adults were more likely to develop breast cancer after menopause. And in yet another report, some of the same researchers found that overweight women have an increased risk of stroke. Other studies have linked obesity with gallstones, noninsulin-dependent—or Type II— diabetes and joint degeneration. But in most of these studies, the relative risk conferred by carrying some extra weight was less than 2.0, which means that fat women were not even twice as likely to die or suffer breast cancer or stroke than their thinner counterparts. In epidemiological terms, this just isn’t much.
The Risks of Dieting
So if obesity confers only a modest increase in mortality, what about the risks of striving to be thin? Extreme diets are known to pose health risks by depleting the body of vitamins and nutrients. But what about the new wonder drugs? They, too, can be dangerous. By now, most people have heard of the demise of the diet-drug combo fen-phen (fenfluramine/phentermine). Fen-phen crashed and burned last September when Wyeth-Ayerst Laboratories took half of the
duo—fenfluramine—off the market at the behest of the Food and Drug Administration. The decision followed reports that some women who had taken fenfluramine developed abnormalities in their heart valves, apparently because the drug elevated blood levels of the neurotransmitter serotonin, the same neurochemical boosted in the brain by Prozac. Wyeth-Ayerst also pulled fenfluramine’s chemical cousin, dexfenfluramine (Redux), from pharmacy shelves. In the aftermath of fen-phen, Knoll Pharmaceuticals delayed marketing its new drug sibutramine (Reductil), which increases brain levels of serotonin and another neurotransmitter, noradrenaline. And on March 13, an FDA advisory committee deadlocked over recommending Hoffmann–La Roche’s orlistat (also called Xenical), which blocks the enzymes that break down fat in the intestines, allowing fat to pass through the gut undigested. The panel said it was confounded by evidence that the drug might cause or exacerbate breast cancer.
So I’m back to where I was when I first saw the New England Journal editorial. Given the current state of affairs, no wonder we’re all confused. Depending on your state of mind, you can
find enough scary medical evidence to get you back to eating rabbit food or sufficient uncertainty to justify an apologia for staying adipose. The bottom line is that researchers still don’t know why some of us are fatter than others. The interpersonal differences in body fatness can’t be explained by food intake, physical activity, genetics or metabolism alone. Some researchers argue that drugs such as fen-phen, sibutramine and orlistat will never eliminate obesity, because the system of body-weight maintenance is like a balloon: pinch it at one end, and it will compensate by swelling at the other. In the January issue of the American Journal of Clinical Nutrition, Jules Hirsch of the Rockefeller University wrote that the mechanisms that determine body weight are carefully balanced. Accordingly, taking a drug to reduce hunger might just cause a reduction in metabolism to save energy, and a drug that ramps up metabolism just might make someone eat more to keep up. So, is it time to join the National Association to Advance Fat Acceptance? That’s up to you. Myself, I draw comfort from a study published in JAMA last year by the Cooper Institute for Aerobics Research in Dallas that found that fat people who exercised on a regular basis were less likely to die prematurely than thin people with poor physical fitness. So I’m going to continue to Jazzercise, swing dance and scuba dive— and try to eat moderately and well. I’m not going to take any more diet drugs, but I’m also not going to give up the good fight to be healthy.
What women in their 70s and up need to know?
Medical studies have shown that having pets can lower blood pressure, shorten hospitalstays and encourage social interaction among older people. Call your local animalshelter for more information about adopting a pet.
U.S. DEATHS in 1995 from cardiovascular disease:455,152 men505,440 women from cancer(all forms):281,611 men256,844 women
Choose one pharmacy that you can go to consistently for all your medications. If the pharmacists get to know you,they’ll be aware of all the drugs you’re taking and may be able to alert you if you begin taking medicines that aren’t compatible with one another.
Are you not enjoying retirement? Planning some new activities could make you feel better. But if not, speak up—you may be suffering from depression. Your doctor might be able to help by prescribing antidepressant medication or recommending a psychotherapist.
Essential medical exams for women in their 70s and up
Every year 50,000 to 70,000 Americans die from diseases that could have been prevented by vaccinations. The Centers for Disease Control and Prevention (CDC) recommends that adults age 65 and older receive vaccinations against tetanus every 10 years, an annual shot against influenza and a vaccine against pneumonia. The Administration on Aging also suggests that people who have blood-clotting disorders or who require kidney dialysis be vaccinated against hepatitis.COST: The cost for each vaccination is different butshould be covered by insurance.
Although eyes commonly weaken with age, many diseases of the eye can be effectively treated if caught early. The National Eye Institute recommends an eye exam once every two years for everyone older than 60 and once a year if you’re diabetic. The eye doctor will test your eyesight and your glasses and should check for glaucoma, cataracts and macular degeneration(the deterioration of the central part of the retina). If you begin to notice changes in your eyesight, the National Institute on Aging suggests adding brighter lights in your home—it may help you see better for reading and other tasks and should help prevent accidents.COST: $50–$100
Losing your teeth is not a natural part of aging. Scheduleannual dental appointments to keep your teeth healthy.And if you wear dentures, you still need to go in: have yourdentures professionally cleaned and adjusted for fit regularlyor if your weight changes by more than 10 pounds or so.COST: $60–$200
Don’t suffer in silence from urinary incontinence. At least one out of 10 people over age 65 in the U.S. suffers occasional lack of bladder control. If you begin to experience problems, see your doctor: incontinence is very often treatable.
Women who smoke have 6% less bone mass by age 80 than women who don’t smoke.
For people between 65 and 84 years old, falls are the second leading cause of death from injury and the foremost cause for those 85 years and older.Fractures occur in 5 percent of all falls; hip fractures are the most serious of injuries and result in the greatest number of deaths.
HEART DISEASE SCREENING
Doctors rely on a variety of tests to look for heart disease,the leading killer of women (and men) in the U.S. Have your cholesterol and blood pressure checked regularly. If yourdoctor suspects heart disease, she may refer you for one or several of the following tests: an electrocardiogram (which measures electrical activity of the heart); a stress or treadmill test (which records heartbeat during exercise); nuclear scanning (which can show damaged areas of the heart); or coronary angiography (which examines coronary arteries).COST: Variable
COLORECTAL CANCER SCREENING
Physical inactivity and older age are two risk factors associated with cancers of the colon and rectum, so continue to schedule regular exams to screen for these diseases. The American Cancer Society (ACS) recommends a few options,including a digital rectal examination, fecal occult blood tests, sigmoidoscopy (inspection of the lower largeintestine) and colonoscopy (inspection of the entire large intestine); ask your doctor which is appropriate for you.Symptoms of colorectal cancer may include changes in bowel habits for more than a few days, rectal bleeding and,in some patients, cramping or stomach pain.COST: Variable; be sure to find out which tests are covered by your insurance.
According to the National Cancer Institute, one in 14 women will develop breast cancer by age 70; by age 80 the number increases to one in 10. Schedule an annual mammogram—the earlier you detect breast cancer, the better.COST: $50–$150
SKIN EXAMKeep up your annual skin examinations to check for skin cancer. In addition, your skin may be more sensitive these days—to sunlight, bruises, sores and dryness. Be aware of exposure to the elements and keep your skin clean and well moisturized.COST: Included in a routine visit to the doctor.
BONE DENSITY EXAM
Some 20 million American women are affected by osteoporosis.Ask your doctor if you should have a bone density scan, which is an x-ray of your bones that can detect bone loss. Your doctor may recommend hormone therapy or other drugs, diet changes or exercise to increase the mass and strength of your bones. COST: $100–$300. Medicare pays in some states. But beware,not all private insurers will cover this test; ask before you go to the doctor.
PELVIC EXAM AND PAP TEST
Although your risk of developing cervical cancer doesn’t increase with age, the risk of ovarian cancer does. Half of all women diagnosed with ovarian cancer are older than 65,according to the ACS, and the pelvic exam is the only way to catch this disease early. The ACS recommends an annual pelvic exam and Pap test to screen for these cancers.COST: Pelvic exam $40–$100; Pap test $20–$60. Usually covered by insurance.
More than one third of all Americans between the ages of 65 and 74 experience some natural hearing loss, but you can get help. If words become hard to understand or if you begin to hear hissing or ringing noises in the background,find an audiologist and have your hearing tested.The audiologist will measure your ability to hear sounds at different pitches and volumes and may suggest a hearing aid to help amplify the sounds coming into your ear.And because there are different types of hearing loss,there are different types of hearing aids.COST: Hearing test $10–$100
Why Women Live Longer than Men?
Women around the world have a survival advantage over men—sometimes by as much as 10 years. What gives them the upper hand?
It is a fact of life that men enjoy certain physical advantages over women. On average, men are stronger, taller, faster and less likely to be overweight. But none of these attributes seem to matter over the long haul. For whatever the physical virtues of maleness, longevity is not among them. Women, as a group, live longer than men. In all developed countries and most undeveloped ones, women outlive men, sometimes by a margin of as much as 10 years. In the U.S., life expectancy at birth is about 79 years for women and about 72 years for men. The gender discrepancy is most pronounced in the very old: among centenarians worldwide, women outnumber men nine to one. The gender gap has widened in this century as gains in female life expectancy have exceeded those for males.The death rates for women are lower than those for men at all ages—even before birth. Although boys start life with some numerical leverage—about 115 males are conceived for every 100 females—their numbers are preferentially whittled down thereafter. Just 104 boys are born for every 100 girls because of the disproportionate rate of spontaneous abortions, stillbirths and miscarriages of male fetuses. More boys than girls die in infancy. And during each subsequent year of life,mortality rates for males exceed those for females,so that by age 25 women are in the majority.For us, these statistics raise two questions: Why do men die so young? And why do women die so old? From the outset we would like to admit that we have no definitive answers to these questions. But the available evidence implicates behavioral as well as biological differences between the sexes, differences in the effects of medical technology, as well as social and psychological factors. Ultimately, our investigation of the gender gap in life span has led us to posit an evolutionary explanation, one that suggests that femalelongevity is more essential, from a Darwinian perspective, than the prolonged survival ofmales. The good news is that in spite of this evolutionary imperative, the gap between male and female life expectancy may now be narrowing.The bad news is that some of this convergence may be the result of women suffering more from what used to be considered “male” diseases.Toxic TestosteroneComparison of the death rates for men and women in the U.S. at various ages reveals gender differences in mortality patterns.Although death rates are higher for males than females at all ages, the difference between the sexes is more pronounced at certain stages of life.Between 15 and 24 years, for example, the maleto-female mortality ratio peaks because of a sudden surge in male deaths with the onset of puberty.During this period, men are three times more likely to die than women, and most of the male fatalities are caused by reckless behavior or violence.Motor vehicle accidents are the most common cause of death for males in this age group,followed by homicide, suicide, cancer and drowning.Interestingly, a surge in male mortality hasbeen observed in other primates at a similar stage in life: in young adult male macaques, for example,rates of death and “disappearance” are high compared with those of female macaques.The difference between male and female mortality declines until late middle age, when the mortality ratio plateaus. In the 55- to 64-year-old age group, behavior-related fatalities are still among the most common causes of death for men and are still much higher in men than in women. Men of this age are more than twice as likely as women to die in car accidents, for example, and almost four times as likely to take theirown lives. Illnesses related to smoking and alcohol consumption also kill more men than women in this age group. But heart disease is the main cause of the gender gap here. Men experience an exponential rise in the risk of heart disease beginning in their 40s; in contrast, women’s risk of dying from heart disease does not begin to increase until after menopause, and it approaches the male risk only in extreme old age. Although the gender gapin this age group is smaller than the one described for young adults, the number of people affected by it is far greater. Whereas accidents claim the lives of 45 of every 100,000 young adult males annually, heart disease—the leading cause of death in men and women alike—kills 500 of every 100,000 men between the ages of 55 and 64 every year.Experts suspect that gender differences in mortality patterns may be influenced at least in part by sex hormones, namely the male hormone testosterone and the female hormone estrogen. The conspicuous peak in the sex-mortality ratio at puberty, for example, coincides with increased testosterone production in men. Because the male hormone has been linked with aggression and competitiveness as well as libido, some researchers ascribe this spike in male mortality to “testosterone toxicity.” Later in life, testosterone puts men at risk biologically as well as behaviorally. It increases blood levels of the bad cholesterol (known as LDL, for low-density lipoprotein) and decreases levels of the good one (HDL, forhigh-density lipoprotein), putting men at greater risk of heart disease and stroke.Estrogen, on the other hand, has beneficial effects on cardiovascular health,lowering LDL cholesterol and increasing HDL cholesterol. A recent study at the University of Washington suggests that estrogen may exert these effects by regulating the activity of liver enzymes involved in cholesterol metabolism. Estrogen is also an antioxidant—that is, it neutralizes certain naturally occurring,highly reactive chemicals, called oxygen radicals, that have been implicated in neural and vascular damage and aging. Emerging evidence suggests thattreatment with estrogen after menopause reduces a woman’s risk of dying from heart disease and stroke, as well as her risk of dying in general. Estrogen therapy has also been shown in some studies to delay the onset of Alzheimer’s disease.It is important to note that with the exception of this evidence regarding estrogen therapy, the relation between sex hormones and mortality patterns is still speculative. Furthermore, any attempt to explain mortality patterns must include the recognition that these trends are relatively recent. As the graph on the next page shows, the two divergences we have been discussing did not emerge until the middle of the century. Before that time, the sex-mortality ratio was constant across age groups for which data are available. The recent changes can probably be accounted for by two societal factors: improvements in obstetrical care, which have dramatically reduced women’s risks of dying in childbirth, and an increased availability of guns and cars,which has contributed to more accidental and violent deaths in young males.Historical Advantage Although the reasons women live longer than men may change with time, it seems likely that women have been outliving men for centuries and perhaps longer. Even with the sizable risk conferred by childbirth, women lived longer than men in 1900, and it appears that women have outsurvived men at least since the 1500s, when the first reliablemortality data were kept. Sweden was the first country to collect data on death rates nationally; in that country’s earliest records, between 1751 and 1790, the averagelife expectancy at birth was 36.6 years for women and 33.7 years for men.Death rates in less developed countries, whose citizens have limited access to cars, guns and maternalcare, also provide a measure of mortality before modernity. At present,the only countries in which male life expectancy exceeds that for females are those with longstanding sexual discrimination—including Bangladesh, India and Pakistan—where social pressures and practices such as female infanticide and bride-burning result in unique “losses” of females.The fact that women live longer than men does not, however,mean that they necessarily enjoy better health. It could be that women live with their diseases,while men die from them. Indeed,there is a difference between the sexes in disease patterns, withwomen having more chronic nonfatal conditions—such as arthritis,osteoporosis and autoimmune disorders—and men having more fatal conditions,such as heart disease and cancer.Survival of the Fittest To understand better the forces that control human aging and longevity, we have tried to determine whether the longer life span of females might be part of some grand Darwinian scheme. Gender differences in longevity have been observed in other members of the animal kingdom: in fact, in almost all species that have been observed in the wild, females tend to live longer than males. Female macaques live an average of eight years longer than males, for example, and female sperm whales outlive their male counterparts by an average of 30 years.It seems that a species’ life span is roughly correlated with the length of time that its young remain dependent on adults. We have come to believe that when a significant, long-term investment of energy is required to ensure the survival of offspring, evolution favors longevity—in particular, female longevity.Indeed, we believe that the necessity for female longevity in the human reproductivecycle has determined the length of the human life span.We start with the assumption that the longer a woman lives and the more slowly she ages, the more offspring she can produce and rear to adulthood. Longlived women therefore have a selective advantage over women who die young. Long-lived men would also have anevolutionary advantage over their shorter-lived peers. But primate studies suggestthat men’s reproductive capacity is actually limited more by their access to females than by life span. Hence, the advantage of longevity for men would notbe nearly as significant as it is for women.And because males historically are not as involved in child care as females,in the not so distant evolutionary past the survival of a man’s offspring dependednot so much on how long he lived as on how long the children’s mother lived.One might think that the existence of menopause halts the transmission of a woman’s genes and thus contravenes the evolutionary argument for female longevity. We think just the opposite:menopause confers a selective advantage and promotes longer life by protecting females from the increased mortality risk associated with childbirth at advanced age. Even today this increase in risk is considerable: a woman in her 40s is four to five times more likely todie in childbirth than a 20-year-old.When menopause evolved, maternal mortality would have been much greater.If offspring require a significant maternal investment of time and energy tosurvive—which human children most certainly do—then there probably comes a point in a woman’s life when it is more efficient to pass on her genes by caring for the children and grandchildren she already has than by producing and nurturing more children, risking death and the death of her existing children in the bargain. The argument that menopauseis an evolutionary adaptation was first developed in 1957 by George C. Williams, now at the State University of New York at Stony Brook,and recent anthropological studies have supported it. Because human children are dependent for such a long time, continued health and longevity may enhance older women’s contribution to the gene pool even when they can no longer reproduce.In our own studies of centenarians,we have found that a surprising proportion of women who lived to be 100 or more gave birth in their 40s. One of our subjects had even had a child at the age of 53.We found that, overall, 100-year-old women were four times as likely to have given birth in their 40s as a control group of women, born in the same year, who died at the age of 73. This observation reinforces our suspicion that longevity is linked with fecundity at an advanced age. Of course, we do not mean that having a baby in middle age makes a woman live longer. Rather, it seems that the factors that allow certain older women naturally to conceive and bear children—a slow rate of aging and perhaps also a decreased susceptibility to the diseases associated with aging—also improve these women’s chances of living a long time. We propose that women’s longevityedge over men may simply be a by-product of genetic forces that maximized the length of time during which women could bear and raise children and perhaps assist with grandchildren as well.Moreover, male longevity may simply be a function of the fact that men mustcarry the genes that ensure longevity to pass them on to their daughters. Thus,the necessity of female longevity in the human species may be the force that has determined the natural life span for both men and women.The Secret to Living Longer If female longevity is the product of evolutionary forces, then one might wonder what physiological mechanisms have evolved to support the preferential survival of women over men. As we have mentioned, sex hormones are thought to be important factors in determining the relative susceptibilities of the genders to aging and disease. Less obvious is the contribution that menstruation might make to longevity. Because of the monthly shedding of the uterine lining premenopausal women typically have 20 percent less blood in their bodies than men and a correspondingly lower iron load. Because iron ions are essential for the formationof oxygen radicals, a lower iron load could lead to a lower rate of aging, cardiovascular disease and other age-related diseases in which oxygen radicals play a role. Indirectsupport for this theory comes from studies at the University of Kuopio in Finland and the University of Minnesota Medical School. In these studies, male volunteers who made frequent blood donations had less oxidation of LDL cholesterol—a key step in the development of atherosclerosis and heart disease.Women also have a slower metabolism than men—a distinction that makes them more prone to obesity. But there may also be an inverse relation between metabolic rate and life span. Evidence of this link comes from animalstudies of food restriction, which slows metabolic processes: in experiments sponsored by the National Institute on Aging, monkeys that ate 30 percent less of the same diet as their free-feeding peers seemed to age more slowly.Studies of so-called clock genes in microscopic worms have also demonstrated the connection between metabolic rate and life span. Siegfried Hekimi of McGill University has observed that worms with particular mutations in these geneslive five times as long as normal animals and have much slower physiological functions. Although it is still not known why men’s metabolism rates are faster than women’s, it is becoming clear that this difference is present almost from themoment of conception, when male embryos divide faster than female ones. The faster metabolic rate may make men’s cells more vulnerable to breakdown, or it may simply mean that the male life cycle is completed more promptly than the female one.Finally, chromosomal differences between men and women may also affect their mortality rates. The sex-determining chromosomes can carry genetic mutations that cause a number of life-threatening diseases, including muscular dystrophy and hemophilia. Because womenn have two X chromosomes, a female with an abnormal gene on one of her X chromosomes can use the normal gene on the other and thereby avoid the expression of disease (although she is stilla carrier of the defect). Men, in contrast,have one X chromosome and one Y chromosome, and so they cannot rely on an alternative chromosome if a gene on one of the sex chromosomes is defective.This disadvantage became more ominous when, in 1985, researchers at StanfordUniversity reported the discovery on the X chromosome of a gene critical to DNA repair. If a man has a defect in this gene, his body’s ability to repair the mutations that arise during cell division could be severely compromised. The accumulation of such mutations is thought to contribute to aging and disease.There is also increasing interest in women’s second X chromosome as a longevity factor in and of itself. Although one of the two Xs is randomly inactivated early in life, the second X seems to become more active with increasing age. It may be that genes on the second X“kick in” and compensate for genes onthe first X that have been lost or damaged with age. This compensation could have a sizable influence, as it appears that roughly 5 percent of the human genome may reside on the X chromosome.In recent years the X chromosome has also become the focus of the search for genes that might directly determine human life span.Closing the Gender Gap Men and women alike have seen profound gains in life expectancy in this century. Since 1900, the average national increase in life expectancy in developed countries has been 71 percent for womenand 66 percent for men. This increase cannot be explained by physiological or evolutionary theories. Rather, swift changes in knowledge of health and disease, changes in lifestyle and behavior,and advances in medical technology have greatly improved the chances of both sexes’ living to old age.In the past two decades, however,there has been a notable deceleration in the extension of life expectancy in women. The reasons for this decline are still being debated.Some researchers feel that women in developed countries are close toreaching the natural limits of human life span, and so their gains in life expectancy must inevitably diminish.But some sociologists have discounted this reasoning, pointing instead to women’s changing roles in society. As more women have taken on behaviors and stresses that were formerly confined to men—smoking, drinking and working outside the home—they have become more likely to suffer from diseases that were traditionally considered “masculine.” Mortality from lung cancer, for example,has almost tripled in women in the past two decades. Smoking seems to be the “great equalizer” for men and women:current actuarial data from Bragg Associates in Atlanta show that on average middle-aged female smokers live nolonger than male smokers do.In part because of these factors, men’s and women’s death rates in the U.S. have begun to converge in the past 20 years.But it is primarily the reduction in male mortality, as opposed to the increase in female mortality, that is narrowing thisgender gap. In general, the higher a nation’s level of social and economic development,the greater the life expectancy for both men and women and the greater the convergence in the two figures. Research on sex hormones, sex chromosomes and gender-specific behavioris sure to further understanding of the human body well beyond the questions posed by the longevity gender gap. In exploring this intriguing phenomenon,investigators will undoubtedly find clues to how both men and women can live longer and more healthy lives.
It’s hard to envision a thin, athletic woman as a hip fracture victim waiting to happen. Unfortunately, research shows that women athletes who often diet and don’t get enough calcium have among the highest risks for developing osteoporosis when they reach their 50s and 60s. Some young female athletes are also at risk because they lose so much body fat that they stop having their menstrual periods, which lowers their estrogen levels and leads to bone loss. Osteoporosis is characterized by decreased bone mass and an increased risk of broken bones. According to the U.S. National Osteoporosis Foundation, more than 28 million people in the U.S. are at high risk of developing the potentially crippling disorder—and most of them are women. That figure is predicted to jump to 41 million by 2015, when women in the baby boom generation will be beyond menopause. KARYN HEDE, special correspondent for SCIENTIFIC AMERICAN, discusses what women should know about osteoporosis with DONALD P. MCDONNELL, Ph.D., associate professor of pharmacology and cancer biology at Duke University Medical Center, and ROBERT LINDSAY, M.B.- Ch.B., Ph.D., chief of internal medicine at Helen Hayes Hospital in West Haverstraw, N.Y. McDonnell’s research focuses on a new class of compounds called selective estrogen receptor modulators (SERMs), which offer hope for preventing and treating osteoporosis without the side effects of estrogen. Lindsay
is founding director of the metabolic bone disease unit at St. Luke’s–Roosevelt Hospital in New
York City and is the author of over 200 publications on osteoporosis and estrogen replacement therapy.
What causes osteoporosis? And why are women particularly prone to the disease?
MCDONNELL: To answer that, I need to describe what usually happens in normal bone. Bones are very complex and dynamic organs. There are basically two types of bone cells: osteoblasts,
which make bone, and osteoclasts, which break down bone. Normally, these cells function in concert throughout life to resorb old, worn-out bone and replace it with new bone. In osteoporosis, this balance gets thrown off in favor of the osteoclasts. The hormone estrogen, which is present in much greater quantities in women than in men, regulates the bone deposition process. A number of sex hormones may be involved in maintaining bone mass. In men, estrogen and androgens are involved. Men have more estrogen than women after menopause, so they are relatively more protected. But men do get osteoporosis, just in lower numbers. Women have two stages of bone loss: from about age 35 to menopause, and after menopause. We don’t really understand the first stage, although estrogen levels have already begun to drop during that time of life. But after menopause, osteoporosis results from the lack of estrogen.
What is known about the role of estrogen in maintaining healthy bones?
MCDONNELL: This is a case in which the clinical data have been way ahead of basic science. For years, all we knew was that when you put women on hormone replacement therapy, they stop losing bone and actually regain a small bit of bone mass. But we’ve had some revealing developments in the laboratory within the past few years. It’s becoming clear that estrogen binds to estrogen receptors in bone progenitor cells, the cells that give rise to the osteoblasts and osteoclasts. After menopause, a lack of estrogen actually stimulates production of both cell types—but with a net increase in osteoclasts, which results in a net loss of bone.
LINDSAY: We still do not understand exactly how estrogen controls skeletal remodeling. But when women go through menopause, the normal bone-remodeling process goes crazy. After the ovaries stop secreting estrogen, the number of sites where the bone cells are breaking down old bone and making new bone increases. Theoretically, the amount of old bone removed should be exactly equal to the amount of new bone laid down. But after menopause there’s an imbalance between bone resorption and bone formation in favor of resorption. As a consequence, after each remodeling cycle you end up with slightly less bone.
Who is at risk for developing osteoporosis?
LINDSAY: The major risk factors are age and race: Caucasian and Asian women who have reached menopause have the greatest risk. Having a family history of osteoporosis increases
risk because there’s a genetic component to the overall amount of bone you start with as an adult. Beyond that, other risk factors are a thin physique, smoking, excessive alcohol consumption and a history of low calcium intake. In addition, some medications, such as steroids, the anticoagulant heparin and anticonvulsants, can accelerate bone loss. Lowering Your Risk
So what should women with these risk factors do?
LINDSAY: If you have three or more risk factors, you ought to think seriously about having a bone-density scan around the time of menopause. A bonedensity scan, technically called dualenergy x-ray absorptiometry (DXA), is used to measure bone mineral density in the spine, hip and wrist, the most common sites for osteoporotic fractures. Bone scans take just a few minutes and result in very low x-ray exposure—about one tenth that of a standard chest x-ray.
Women with low bone density at menopause are very likely to develop fractures; the lower your bone density, the higher your risk. Measurements are based on the mean bone density of a
young woman at peak bone mass. Based on the results of the scan, a patient and her physician can decide among several courses of action. If a woman has high bone density, greater than one standard deviation above normal, her doctor might say, “You don’t need to worry; you’re not
going to get osteoporosis.” To a woman with average bone density who is just entering menopause, a physician might say, “We don’t know whether you are going to lose bone or not, so come back and get a measurement in two to five years.” To get the best reading, that woman should go back and have the measurement done at the same place, on the same machine and preferably with the same technician. If a woman’s bone density is a little lower than average for her age—greater than one standard deviation below normal—and she’s 55 years old, her doctor
might say, “Here are things you can do to change your lifestyle: stop smoking, reduce your alcohol intake, increase your calcium intake and increase your physical activity.” Moderate physical activity not only helps bones grow stronger, it also reduces the risk of falling and breaking a bone better than anything else. That woman’s physician would also want to measure her bone density again in a couple of years to see whether she was losing bone rapidly. A woman with bone density lower than 2.5 standard deviations below normal is at particularly high risk for a fracture and should consider pharmacological intervention.
How accurate is bone-density scanning in predicting a woman’s future risk of a bone fracture?
LINDSAY: Bone density is a better predictor of fracture than cholesterol is for heart attack or blood pressure is for stroke. Roughly speaking, a 10 percent reduction in bone density doubles
a woman’s risk of fracture after menopause. Should premenopausal women have their bone density checked?
LINDSAY: By and large, premenopausal women don’t need to have a bonedensity measurement unless they have very clear risk factors for osteoporosis, such as anorexia and problems with the
function of their hypothalamus, a region of the brain that’s involved with hormone regulation. The time for women to consider a bone scan is somewhere around the perimenopausal years, from the early 40s to the early 50s.
What can premenopausal women do to reduce their future risk of osteoporosis?
LINDSAY: The key to preventing osteoporosis— and many other diseases of aging— is a healthy way of life, particularly a good diet high in calcium. In general, nonpregnant women should take in between 1,000 and 1,500 milligrams of calcium per day, whether in food or as a dietary
supplement. The National Health and Nutrition Examination Studies found that the average calcium intake in the U.S. is only about 600 milligrams a day. The elderly who are homebound or have chronic illnesses must also ensure that they get enough vitamin D, which helps the body use calcium. Most multivitamins contain vitamin D; intake should be five to 7.5 micrograms a day. Being physically active is also important. Having regular periods is crucial because young women who don’t menstruate usually have low estrogen levels, which can mean losing bone mass. And here’s yet another reason why a woman should stop smoking: it’s as bad for your bones as it is for your lungs and heart. Treating Osteoporosis Estrogen is frequently prescribed for menopausal and postmenopausal women to prevent osteoporosis. Yet the use of estrogen has been associated with an increased risk for breast cancer and cancer of the endometrium, the lining of the uterus.
Is estrogen still the best treatment for osteoporosis?
MCDONNELL: Estrogen has been on the market now for 50 years, and it has an excellent record not only in treating osteoporosis but also in reducing a woman’s risk of cardiovascular
disease. It also reduces other unwanted side effects of menopause, such as hot flashes. There is a small increase, however, in the incidence of breast cancer among women who take estrogen, although new evidence suggests that women who take estrogen have a lower overall mortality rate. So on balance, the beneficial effects of estrogen for most women greatly outweigh its potential risks. Estrogen with progestin, in a combination called hormone replacement therapy, reduces the risk of endometrial cancer. Still, the breast cancer issue remains at the front of women’s minds.
LINDSAY: The gold standard for treatment of osteoporosis is hormone replacement therapy. If women are already on hormones for other reasons—to control menopausal symptoms or because they are concerned about heart disease—then they need do nothing more. Hormone replacement therapy is the first-line therapy for osteoporosis because it has proved to be
the best protection against bone loss.
Are there other drugs that can protect against bone loss, without estrogen’s side effects?
MCDONNELL: One of the newest therapies is a class of drugs called the bisphosphonates, of which the best known is alendronate, or Fosamax. The bisphosphonates do not work like
hormones. They do not bind to the estrogen receptor in bone progenitor cells; they enter the bone directly. One hypothesis is that the bisphosphonates reduce the activity of osteoclasts,
thereby reducing bone resorption. These agents are very effective in the treatment of osteoporosis. But every drug has a positive side and a negative side. The negative side is that these agents have no beneficial effect on the cardiovascular system and that they do not reduce the other symptoms of menopause, such as hot flashes.
LINDSAY: The people who are most likely to use a bisphosphonate drug such as Fosamax are those who have the highest risk of developing osteoporosis. The problem with Fosamax is that at the higher dose used for treatment, 10 milligrams, it has been associated with some upper gastrointestinal symptoms—heartburn and dyspepsia. That’s why it’s a second-line therapy for most people. And in rare instances, Fosamax can cause esophageal ulcers. A new drug called Evista was approved by the Food and Drug Administration last December for treating osteoporosis.
How does it work?
MCDONNELL: Evista, or raloxifene, is the first approved selective estrogen receptor modulator, or SERM. Other SERMs are now being tested in clinical trials. These drugs function as estrogens
in the bone but not in the other organs. In fact, Evista functions as an antiestrogen in the breast by blocking the estrogen receptor, which can spur breast cancer growth. So although it remains to be proved, SERMs might actually reduce a woman’s risk of breast cancer. Several small studies have shown that SERMs decrease breast cancer by 70 percent. They can also reduce the risk of endometrial cancer. Long-term studies are still needed to see if that holds up over the long run. The SERMs have also introduced totally new issues for women to consider. Evista is only about one half to one third as effective as estrogen in preventing bone loss, and the preliminary data suggest that it doesn’t begin to match up to estrogen in protecting against cardiovascular disease. But new SERMs are in development that are likely to show more promise in this regard. Another downside is that current SERMs not only don’t protect against hot flashes, they actually induce hot flashes—the reason most menopausal women go to their doctors in the first place. On top of all that is the question of how SERMs will affect the estrogen receptors in the nervous system:
Will SERMs decrease cognitive function or increase the risk of Alzheimer’s disease? Those are going to be important issues.
How can SERMs act selectively in some tissues but not in others?
MCDONNELL: When estrogen binds to its receptors in cells, it activates them by converting them from a square shape into a circular shape. The circular shape is then able to complete all
the effects of estrogen in the cell, including turning on some genes. What SERMs do is warp the receptors into new and different shapes. We found that different cells have different abilities
to recognize these shapes. For instance, cells in the breast can recognize only a circle. But bone cells aren’t that choosy. They can recognize either the circular shape or an alternative
shape. So compounds like SERMs that can mold estrogen receptors into another shape can activate the receptors in the bones but can also block the receptors in the breast and endometrium. Using this approach, I believe we will eventually be able to “dial in” certain properties of estrogen, such as protection against heart disease, and “dial out” others, such as its
ability to contribute to breast cancer and endometrial cancer.
Taking into consideration the pros and cons of SERMs, who should take them?
MCDONNELL: I think SERMs are going to appeal to women who are skeptical of hormone replacement therapy because of the side effects or who have a family history of breast cancer.
SERMs might be effective as chemopreventatives against breast cancer and endometrial cancer. Perhaps most important, these new drugs are going to increase women’s overall awareness of
hormone replacement therapy. When women have more options, they will have more incentive to seek some type of therapy during and after menopause. The hormone calcitonin is sometimes offered to women as a treatment for osteoporosis.
What is calcitonin?
LINDSAY: Calcitonin is normally produced by the thyroid gland to help the body maintain appropriate concentrations of calcium. It is given either as a subcutaneous injection or as a nasal spray, because it is a protein and would be broken down in the stomach if taken by mouth. Before SERMs, calcitonin was the third-line choice for the treatment of osteoporosis because it is not as potent as either alendronate or hormone replacement therapy. Its major advantages are that it is safe and the side effects are modest: some nasal irritation and flushing of the face in the first few weeks of use. It’s been around for a long time, and there are no major side effects associated with it. It’s used mainly for those who can’t or won’t take hormones and who can’t take alendronate because of gastrointestinal complaints. If some people have a genetic predisposition to osteoporosis, what will it mean for women if a gene for osteoporosis is found?
LINDSAY: The genetics of osteoporosis is a fascinating field that is growing rapidly. The major approach has been to look for candidate genes and then to evaluate whether different forms of those genes are associated with differences in bone density or the risk of a fracture. The genes that have been looked at include the genes for collagen, which makes up cartilage; the vitaminD
receptor; and the estrogen receptor and various growth factors. The very fact that there are all these candidate genes suggests that there may be no single gene that will be useful in a clinical test for osteoporosis risk. Some of the genes are seen more frequently in people who develop fractures, but generally they confer only modest differences in risk. Another approach has been to look at osteoporosis that runs in families to see if you can identify a common gene in those families. Very little has come out of that work thus far. I think a genetic test would be of considerable value in terms of guiding lifestyle. We know that lifestyle during the time of young adult life is responsible for about 10 to 20 percent of the variability in bone mass. If we knew there was a gene that had a high prevalence in a family with osteoporosis, physicians could encourage women in such families to build as much bone as possible while they are young through a healthy way of life and getting plenty of calcium. On the Horizon
What are the most promising therapies coming in the next five years?
MCDONNELL: In my mind, we’re going toward what I call designer therapies. A woman may go to her doctor and have a family history of osteoporosis but no problems with cardiovascular
function. A SERM might be fine for her because she gets protection against bone loss, in the organ where she is most at risk. She’s not overtreated. Women themselves are going to decide
the market. A woman might say to herself, “SERMs produce hot flashes, so I’ll take estrogen for a few years and then switch over to Evista.” Women want choices; they want to be much more involved in the treatment of their own menopause.
LINDSAY: I think the most interesting work is being done with agents that might repair the skeleton. Researchers first noted in 1929 that parathyroid hormone can add bone to the skeleton. But that finding was basically ignored until the 1970s, when parathyroid hormone was first synthesized in the lab. Now the first controlled clinical trials of parathyroid hormone as a treatment for osteoporosis have appeared. Last August we published a paper in the journal Lancet outlining the results of a threeyear study of this hormone. We found that it produces a dramatic increase in bone density—much larger than you see with any of the current therapeutic options. It also appears to reduce the number of spinal fractures. So parathyroid hormone or an analogue might be developed for the treatment of osteoporosis. I think there’s a very rosy outlook for osteoporosis. We have the mechanisms now for diagnosing it, we have some treatment options, and over the next few years we can expect more and better treatments. With all of this, the disease ought to disappear in the next millennium.
At More Risk for Alzheimer’s?
Scientists are studying how genes and gender interact in Alzheimer’s disease
Now and again we all forget where we left our glasses or what we hurried into the kitchen to retrieve. As we get older, these events seem to increase in frequency. But Alzheimer’s disease is more than mere forgetfulness. It is a degenerative disease of the brain that causes cognitive dysfunction, behavioral changes and dementia. The disease, which affects an estimated four million Americans, eventually robs its victims of their memories and their ability to reason. And
Alzheimer’s appears to affect women more frequently than men. The finding that women might have an increased susceptibility, particularly women with a certain genetic background, has begun to provide crucial clues about the underlying biology of the disease and new insight into its prevention and treatment. Further, a number of small clinical and epidemiological studies have shown that estrogen replacement therapy appears to help protect postmenopausal
women from Alzheimer’s. By exploring how estrogen affects the development and activity of the brain, researchers may uncover new ways to protect people at risk for developing Alzheimer’s disease. Since the turn of this century, life expectancy has been steadily increasing. By 2030, some nine million Americans will be 85 or older. Unfortunately, as a greater proportion of the population survives past 85, the number of people with Alzheimer’s disease will rise. The prevalence of the disease increases dramatically after age 65, rising from 4 to 6 percent at 65 to 15 to 20 percent at 75 and 30 to 40 percent at 85. This century has seen dramatic increases in the life expectancy of women compared with that of men. With an elevation of women’s social status and the elimination of many of the risks of pregnancy, women are surviving as many as three to 10 years longer than men. Because women are living longer, they are at greater risk for developing Alzheimer’s disease—a situation that is re- flected in the higher prevalence rates in women. Yet studies examining the incidence of Alzheimer’s—how many people are diagnosed a year— offer conflicting results. Some show higher rates for women; others find no difference. Researchers think the disparity in these incidence studies might re- flect the fact that the disease is caused by multiple genes interacting with different environmental influences. The major risk factors associated with Alzheimer’s disease include age, genetic predisposition and gender. But the idea that gender on its own may increase a person’s risk is still controversial. A few preliminary studies suggest, however, that gender may interact with one’s genetic predisposition somehow to influence the age of onset of the disease. In cases of familial Alzheimer’s disease, women are at a higher risk than men of the same age. And they appear to experience an earlier onset. These results suggest that gender may be a risk factor in familial cases of Alzheimer’s, and gender may influence the course of the disease, especially in the
presence of certain genes. Over the past few years, researchers have found that mutations or different forms of a particular gene may occur more frequently in people with Alzheimer’s
than in the general population. In 1992 Alan D. Roses and his collaborators at Duke University found such a relation between one form of the gene for apolipoprotein E (ApoE) on chromosome 19 and an increased risk for late-onset Alzheimer’s. This finding established the APOE gene as a susceptibility gene for the disease. The APOE gene comes in three varieties, called APOE2,
APOE3 and APOE4. Roses and his colleagues demonstrated a relation between the average age of onset and the number of APOE4 copies a person inherits. People who have two copies of APOE4 tend to get Alzheimer’s at an earlier age—sometimes 20 years earlier—than those who have no copies. But Haydeh Payami and her associates at the Oregon Health Sciences University
recently found that the effect of inheriting one copy of APOE4 differs depending on gender. For men, individuals with two copies of APOE4 were at the highest risk for developing Alzheimer’s,
and men possessing one copy, or no copies, had a lower risk. But for women, having one copy of APOE4 appears to be as bad as having two copies—both genetic situations cause an earlier onset of the disease. If scientists can learn how APOE4 affects the age of onset, or how gender influences that mechanism, they may be closer to developing interventions that can delay the disease. Sex and the Brain Alzheimer’s disease is characterized by a progressive decline in memory, orientation, language and communication skills, and the ability to reason. The destruction of critical brain regions starts 20 to 40 years before symptoms are clinically detectable. Ultimately, the disease leads to the loss of increasing numbers of neurons, especially in the hippocampus and cortex—parts of the brain that help to code memories and process information. As increasing numbers of cells in these critical brain regions die, short-term memory fails, and the ability to do familiar tasks begins to decline. In the late 1970s Barbara B. Sherwin, now at McGill University, first linked a loss of estrogen with memory problems in a group of women who had had their ovaries removed. At the time, few people recognized that estrogen—the hormone that activates and regulates the female reproductive system—may have
a number of effects in the human brain, quite apart from its role in reproduction. Then, in the mid-1980s, Howard M. Fillet of the Mount Sinai School of Medicine conducted the first study on the effects of estrogen on cognition in humans. He found that after six weeks of estrogen treatment, three of seven women with Alzheimer’s showed significant improvement in attention, orientation, mood and social interactions. In addition to such prospective investigations exploring estrogen’s effects, several groups of researchers were conducting
retrospective analyses on previous estrogen studies. In the early 1990s Victor Henderson, Annlia Paganini-Hill and their co-workers at the University of Southern California were among the first to report epidemiological evidence suggesting that estrogen may reduce the risk for Alzheimer’s disease. In a larger study conducted in 1996, Henderson and his colleagues analyzed data from a population of nearly 9,000 older women. In studying a subset of about 250 women who had died with Alzheimer’s disease, the researchers found that the risk for developing Alzheimer’s decreased significantly among women who had received estrogen replacement therapy (ERT). And the women who received the highest doses over the longest times were the most protected. Other epidemiological studies have provided further confirmation of the protective effects of ERT. Richard Mayeux and his collaborators at Columbia University studied 1,124 older women who were free of the clinical symptoms of Alzheimer’s. The researchers found that the age of onset for Alzheimer’s was significantly delayed in estrogen users compared with nonusers, and the relative risk was significantly reduced. Women who were on ERT for longer than one year had the greatest risk reduction. None of the 23 women who were taking
estrogen when they enrolled in the study had developed Alzheimer’s by the time the paper was published. And as part of the ongoing Baltimore Longitudinal Study of Aging, conducted by the National Institute on Aging, Claudia H. Kawas and her colleagues at Johns Hopkins University have studied 472 women whose health status has been followed for 16 years. They found that women who take estrogen after menopause reduced their risk of developing Alzheimer’s disease by 54 percent. The Estrogen Link Animal studies are continuing to reveal how estrogen may enhance brain function. Such findings reinforce the results seen in human clinical studies. It appears that estrogen can improve learning and memory by helping to build and maintain
the synapses that connect neurons in the brain. In the 1970s Bruce S. McEwen and
his colleagues at the Rockefeller University first reported that estrogen might have a direct effect on the brains of rats. They had found that estrogen boosts the ability of neurons to relay chemical messages by increasing the levels of acetylcholine, a neurotransmitter involved in learning and memory. A few years later McEwen, Catherine S. Woolley, Elizabeth Gould and their colleagues discovered that estrogen may enhance learning and memory in animals
by helping to build and maintain the synapses through which neurons communicate with one another. Synapses are destroyed in the brains of people with Alzheimer’s disease, a loss that
hampers their ability to learn and remember information. By removing the ovaries from adult female rats, the Rockefeller researchers found that estrogen deprivation causes a loss of synapses in the hippocampus. Treating these rats with estrogen restored their synapses to normal numbers. Perhaps something similar happens in the brains of postmenopausal women who receive ERT. Another pioneer in this area was Dominique Toran-Allerand of Columbia
University. She showed that in developing neurons grown in a culture dish, estrogen stimulates the growth of axons and dendrites, the neuronal structures that form the synaptic connections.
As we learn more about estrogen, we are finding that it can act alone as an important
biological signal. But, more significantly, estrogen also appears to work in a cooperative manner with other classes of signaling molecules to stimulate neuronal growth and activity. Toran-Allerand recently reported that in neurons grown in culture, estrogen increases the production of receptors that bind to nerve growth factor, a hormone necessary for neuronal development and activity. The results suggest that estrogen and nerve growth factor may work together to enhance each other’s biological activities. It is becoming abundantly clear that estrogen has many facets. It plays a key role in growth and repair of neurons in the brain. But it also may help protect nerve cells against damage from free radicals and other cellular toxins. James W. Simpkins and his co-workers at the University of Florida have found that estrogen can directly prevent brain cells from being killed by toxins through an unknown mechanism that does not involve either estrogen receptors or nerve growth factor. Other investigators, including Judes Poirier of McGill University, are studying how ApoE, a cholesteroltransporting protein, may affect the regeneration and repair of neurons. Such animal studies are beginning to suggest how estrogen may protect the brain from destruction by Alzheimer’s disease. ERT or No ERT? Estrogen replacement therapy might not be the answer for everyone. Fortunately, several studies currently under way should help women to make better- informed decisions about ERT as it relates to Alzheimer’s and other diseases. One such study—a part of the Women’s Health Initiative of the National Institutes of Health—is monitoring the health of 25,000 women, some of whom are receiving ERT plus progestin, which appears to reduce estrogen’s cancer risks.
In a few years, the study should provide a clear picture of how ERT is altering the course of Alzheimer’s. A second clinical study, headed by Ruth A. Mulnard of the University of California at Irvine, is examining the effects of ERT on 120 women with Alzheimer’s disease. The results of this study—sponsored by the National Institute on Aging—should be available within a year.
Toran-Allerand adds a note of caution about interpreting the results of these studies. Many, including the NIH’s Women’s Health Initiative, involve the use of Premarin, an estrogen preparation made byWyeth-Ayerst using the urine of pregnant mares. In the future, additional
studies comparing different forms of estrogen may lead to the development of therapies that are more effective and have fewer side effects. As we learn more about estrogen and how it enhances the viability of neurons, we hope to be able to exploit this information to develop better treatments for delaying, and perhaps preventing, this devastating disease.
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