People often ask me what motivated me to lose so much weight (170 lbs). I tell them: “I didn’t want to die; I looked around me and I didn’t see any morbidly obese old people, and I was getting old… and I wanted to live to be older.” I had been gaining weight, and my doctor had been urging me to lose for years. Then, for two visits I was unable to weigh in at his office because his scale only went to 350. So, on the way to work one day in NYC I stopped at the Fulton Fish Market and asked permission to weigh myself on a commercial scale. I was shocked. I weighed 375 pounds. The next week, as I entered my Doctor’s office, he saw me and said, “Have I got a diet for you!!!” I was motivated.
Of course, as I was losing weight (first on Atkins, and later on Bernstein – for diabetics), I wondered how low I would go. I had the luxury to fantasize about this because I was losing weight easily and without hunger. This will happen when you strictly follow a Very Low Carb (≤20g of carbohydrate a day) Way of Eating. I also remember reading about Calorie Restriction (CR) and longevity in Gary Taubes seminal 2007 book, “Good Calories – Bad Calories” (“The Diet Delusion” in the UK). This defining work is a “tough slog” but a “great read” too. Calorie Restriction and its positive association and correlation with longevity are covered in depth in Chapter 13, “Dementia, Cancer and Aging.” Are you motivated yet?
In 2008 the authors of “The Neuroprotective Properties of Calorie Restriction, The Ketogenic Diet and Ketone Bodies,” published online as a NIH Public Access peer-reviewed manuscript here, said, “Obesity is associated with an increased risk of dementia.” They continued, “Low dietary energy intake is associated with decreased incidence of Alzheimer’s and Parkinson’s diseases…and calorie restriction for 6 months improves biomarkers associated with longevity including reduced fasting insulin levels, body temperature and DNA damage.” And “Calorie Restriction might even reduce disease risk and increase lifespan in normal weight subjects.” Also, “Beneficial effects on mental health have been reported as well, with improved mood following calorie restriction of obese diabetic patients.” Each quote cites a study or studies.
The problem with the preceding paragraph is that “all the available information is derived exclusively from animal models.” “Calorie restriction prolongs the lifespan of yeast, roundworms, rodents and monkeys, even when initiated in midlife.” “Moreover, age-related deficits in learning and motor coordination are reduced by calorie restriction in rodents.” “Aged mice exhibited similar improvements in learning tasks…” And, “in parallel, calorie restriction also prevented age-related deficits in…a cellular correlate of memory.” “To date, however, clinical trials looking at the effects of calorie restrictions on brain aging and neurological disease have not been performed [on humans],” say the authors.
The authors continue, “the mechanisms that have been proposed to explain the neuroprotective effects of calorie restriction can be grouped into two general categories: 1) improved mitochondrial function, leading to decreased production or reactive oxygen species [free radicals] and increased energy output; 2) regulation of gene expression, resulting in decreased activity of pro-apoptotic factors and increased levels of neuroprotective factors such as neurotrophins.” In addition, “calorie restriction delays age-related oxidative damage to DNA, proteins and lipids” [the ‘antioxidant effect’], thus “decreasing the mitochondrial production of reactive oxygen species” [again,‘free radicals’].
Back to Taubes: “All this leads us back to the spectacular benefits of semi-starvation on the health and longevity of laboratory animals” (GC-BC: pg. 218). “The calorie-restricted animals live longer because of some metabolic or hormonal consequence of semi-starvation, not because they are necessarily leaner or lighter” (ibid. pg. 219). I’m thinking, that’s encouraging, and I reasonably conclude from this that it’s what I eat now, not how thin I am, that will (may?) determine my health outcome.
Taubes sums it up nicely this way: “The characteristics that all these long-lived organisms seem to share definitively are reduced insulin resistance, and abnormally low levels of blood sugar, insulin, and insulin-like growth factor (IGF). As a result, the current thinking is that a lifelong reduction in blood sugar, insulin and IGF bestows a longer and healthier life. The reduction in blood sugar also leads to reduced oxidative stress and advanced glycation end-products (AGEs) and all the toxic sequelae that follow. The decrease in insulin and IGF also apparently bestows on the organism an enhanced ability to protect against oxidative stress and to ward off other pathogens” (GC-BC pg. 220).
Quoting Taubes again (GC-BC pg. 220): “The most compelling evidence now supporting this hypothesis has emerged since the early 1990s from genetic studies of yeast, worms and fruit flies, and it has recently been confirmed in mice. In all four cases, the mutations that bestow extreme longevity on these organisms are mutations in the genes that control both insulin and IGF signaling.” Then, Taubes quotes the cancer researcher J. Michael Bishop’s 1989 Nobel Prize lecture: “When reduced to essentials, the fruit fly and Homo Sapiens are not very different.” Next week: CR in humans.© Dan Brown 12/15/12