The legendary Audrey Hepburn, celebrated for her role in Breakfast At Tiffany’s, was famously noted for her slender frame. Nonetheless, her delicate appearance concealed a history of significant health struggles, ultimately leading to her passing at the age of just 63.
A prominent scientist now posits that her genes underwent fundamental alterations due to the starvation she faced as a teenager in the Netherlands, which was under Nazi occupation.
According to Dr. Nessa Carey, this connection between a poor diet and genetic changes may provide insight into the growing health crises we face today, including obesity and diabetes.
The coveted figure of Audrey Hepburn can be traced back to the deprivations she experienced during wartime. Her genetic makeup was profoundly altered due to the starvation she endured as a teenager. Health scientists have warned that obesity rates among Australian men could reach 50% by 2030, as conditions of both obesity and diabetes continue to rise.
Born to a Dutch baroness and an English banker, Hepburn was a young girl living in the Netherlands when the German invasion occurred in 1940. She faced tremendous hardship after her older brother was taken to a labor camp and her uncle and cousin were killed.
From November 1944 to May 1945, a grim chapter known as ‘the hunger winter’ in Dutch history unfolded, during which she experienced severe starvation. The German blockade in her region led to widespread malnutrition, resulting in approximately 18,000 fatalities.
At the age of 16, Hepburn resorted to consuming tulip bulbs and attempting to create bread from grass. In the war’s final days, she hid from the Nazis in a cellar.
Hepburn’s slender silhouette (with a waist measurement of only 20 inches) was not achieved through any celebrity diet fad. Instead, it was a consequence of the jaundice, anemia, respiratory issues, and chronic blood conditions she developed during those desperate times.
After enduring fragile health throughout her lifetime, she passed away in 1993, just two months post-surgery for colon cancer. She reflectively stated regarding her hardships, ‘After living for years under the Germans, you swore you would never complain about anything again.’
The health challenges Hepburn faced, including jaundice, anemia, respiratory complications, and chronic blood issues, contributed to her slight stature.
Dr. Carey, an expert in biology and former senior lecturer, has authored a book suggesting that Hepburn’s poor health stemmed from genetic changes brought on by her distressing childhood nutrition.
This phenomena is being illuminated by the evolving field of epigenetics.
We are starting to grasp that our genes are not simply fixed at birth. A significant number can be modified ‘epigenetically’ as a result of our surroundings and dietary intake. Through this process, genes have the potential to be activated or deactivated, and their functional mechanisms can be altered.
Hepburn’s experience serves as one of countless cases among hunger winter victims that have been examined following the war. Their documented histories provide crucial insights into the severe repercussions that poor diets can have. Thanks to meticulous record-keeping in the Netherlands, researchers have tracked individuals there for over fifty years.
In fact, the most recent analysis of these findings, released last week, highlighted a strong correlation between childhood malnutrition and coronary heart disease.
One of the most concerning discoveries indicates that the health of unborn children can be severely compromised by inadequate nutrition in their parents, especially for mothers who are malnourished during the initial three months of pregnancy.
Although the babies born to hunger winter survivors generally had normal birth weights, many have inherited a significant issue: their obesity rates are notably elevated compared to average levels.
Theories propose that malnutrition while in the womb triggers a survival mechanism that prepares the baby’s metabolism for a life filled with scarcity. Such epigenetic changes result in the prioritization of fat storage rather than the development of vital organs like the liver, heart, and brain.
Recent research indicates that individuals born during the hunger winter may experience additional health complications as they age, including a higher likelihood of developing dementia.
Interestingly, some of these repercussions appear to be evident even in the next generations, impacting the grandchildren of the hunger winter survivors. Not only have the children’s genes undergone epigenetic changes, but these detrimental modifications have been inherited across two generations.
Research from the isolated region of Overkalix in northern Sweden also points to the significant influence of fathers’ diets.
This area experienced severe food shortages in the early 20th century due to failed harvests, alternating with periods of abundance during which people would overindulge.
Studies reveal that fathers who consumed excess food before puberty increased the risk of their sons and grandsons developing diabetes-related illnesses, in contrast to peers whose fathers maintained healthier eating habits during this critical time.
Given that Overkalix’s residents share a close genetic relationship, it’s been determined that the metabolic issues in unusually obese children stem from epigenetic alterations.
Though scientists have yet to fully identify all the genes that can be influenced by poor nutrition, a recent discovery from Cambridge University has isolated one gene, Hnf4a, which can be modified in the offspring of mothers with unhealthy diets during pregnancy.
This gene’s alteration is associated with a heightened risk of developing type-2 diabetes, heart disease, and cancer in later years.
Research indicates that Hnf4a is crucial for the pancreas to produce adequate insulin levels, the hormone responsible for regulating blood-sugar levels.
Studies on human tissue suggest that inadequate prenatal nutrition diminishes the function of Hnf4a as children mature, increasing diabetes susceptibility.
Dr. Susan Ozanne, who spearheaded the study, states, “We are beginning to comprehend how prenatal nutrition influences our long-term health through the aging process of our cells.”
However, findings are not entirely pessimistic. Researchers are uncovering ways in which minor dietary adjustments can help protect ourselves and future generations from harmful epigenetic changes.
For instance, recent laboratory studies indicate that expectant mothers consuming a diet abundant in B vitamins found in leafy green vegetables may decrease the likelihood of their children facing cancers of the stomach, colon, and rectum, which rank among the leading causes of death in the western world.
The consensus is that B vitamins enhance the functionality of tumor-suppressing genes within the gut.
For the majority of individuals, this information… Determining the dietary missteps our mothers may have taken during their pregnancies could prove challenging. However, we all have the opportunity to embrace a diet that could shield us from some of the epigenetic issues we may have inherited.
There are two compelling reasons to consider this: first, such a diet is inherently healthy; second, it might also safeguard our unborn children from potential future issues.
Findings published in the journal Clinical Epigenetics indicate that certain chemical components found in foods can activate genes that inhibit tumor growth while silencing those that encourage it.
The foods that have been identified include grapes, tomatoes, tofu, parsley, garlic, turmeric, and the widely recognized health foods, broccoli and green tea.
As Dr. Nessa Carey, the author of the recent book The Epigenetics Revolution, points out, the emerging studies reveal that adhering to a healthy diet transcends personal responsibility. It is, in fact, a commitment to future generations.
“Perhaps the old adage ‘we are what we eat’ doesn’t encompass the full scope of reality.
Perhaps we are also reflections of what our parents consumed, as well as what their parents consumed before them,” she explains.
by Susan Floyd
