Our Longevity Diet

Haven’t been posting much lately, but nothing much new to report. We are thoroughly accustomed to our fasting schedule now, it is totally routine. We began our fast March 5th, 2008. Up until now we have weighed-in around the 4th or 5th of each month, but after this long, it just seems easier to weigh ourselves at the end of each calendar month. So while we are actually five days short of five months, it is ‘close enough’ for our purposes.

Reminding you again that weight-loss was not and is not the motivating force behind our intermittent fasting diet, here are our current weights, compared to when we started this diet and last month’s report:

• Date - My weight (kilos) - Isabel’s Weight (kilos)
• 5 March 2008 - 99.2 - 65.9
• 3 July 2008 - 95.1 - 62.4
• 31 July 2008 - 95.0 - 61.8

Isabel has been as low as 61 kilos, then rebounded a little, but is down from our last report by more than half a kilo. I am down a mere tenth of a kilo from our preceding report, but this is my lowest weight since beginning the diet.

When we began, we were each about 10% over our ideal weights, according to the Body Mass Index charts. Now I’m about 5.5% overweight, while Isabel is about 3% over. We are making no great effort to restrict our calories or increase exercise, and are content to lose a little, or just stay even — just so we don’t keep gaining as we were prior to this diet.

Five months into the regime we still get hungry, but we are accustomed to it. We don’t have the urge to over-eat when it comes time to eat again, and actually seem to get full on less food than we used to eat. We don’t always eat the healthiest foods, but it is nutritious. Today (after weigh-in) was our day to splurge, the last day of the month, so we had big thick juicy steaks cooked on the charcoal grill, with potato chips, sweet corn, roasted onions, and nopales (cactus). For our every-day typical meals, see the ‘April Meals‘ link in the right-hand column.

Scientists have argued for some time now on exactly what mechanism drives aging and death. Two different predominant theories have been competing for the past thirty years: Bust vs. Rust.

The bust-down theory claims that genes are responsible for senescence, and after a roughly fixed time span they trigger cells to break down and cease repairing themselves. Evidence in support of this genetically driven model are the observations that certain species are long-lived, while others die young. Also, among humans, longevity has been seen to run in families. The problem with this theory is that it implies the typical age-span for a species is the result of biological evolution, yet much aging (at least among species such as humans) occurs after reproduction stops. Explaining a mechanism by which a feature can evolve when it does not affect reproductive success has been difficult.

The rust theory, on the other hand, suggests we just wear out. Disease, toxins, and especially free-radical oxidation damage, gradually accumulates until the body is no longer able to repair itself. Evidence in support of this theory includes the observation that calorie restriction (CR) and intermittent fasting (IF) can greatly extend the lifespan of study animals. The best available evidence suggests that these practices may improve the repair mechanisms in the body, hence holding off aging for a while.

But while CR and IF have been shown to extend life by as much as 50% or more, the animals in these studies still die. Clearly, these methods slow the aging process, but do not stop it. Thus many researchers came to believe that a combination of the two theories was probably more-nearly correct. Aging is affected by the environmental factors of the ‘rust’ theory, but the ultimate limits are genetically programmed.

Earlier research has shown that it is possible to greatly extend the lifespan of fruit-flies through  a kind of selective breeding program that controls what age the flies are allowed to reproduce at. Now another study has identified the exact genetic mechanism for aging in flatworms. According to that report:

Comparing young worms to old worms, Kim’s team discovered age-related shifts in levels of three transcription factors, the molecular switches that turn genes on and off. These shifts trigger genetic pathways that transform young worms into geezers.

As part of the research, they exposed some of the worms to environmental stresses such as heat, free-radicals, radiation and disease, and then measured the activity of the elt-3 transcription factor, which they found to be the controlling chemical in aging. None of the stress factors induced changes in elt-3 levels. The researchers conclude that genetically controlled changes in elt-3 are largely responsible for aging in the worms.

If confirmed in other animals, this shifts the balance back in favor of a strongly genetic source for aging, but it also provides a chemical target and pathway for interfering with the aging process. As with most research in this field, it is still way too early to tell — but we see progress is being made.

So far as our personal Intermittent Fasting regime is concerned — we never really expected it would help us live much longer than normal, since we started too late in life to reap the full benefits. At best we can hope for an extra 10% (i.e. living to 88 rather than 80). Our main motivation is the evidence that for those remaining years we are likely to be much healthier under the IF lifestyle than otherwise.

I continue to see references to Fast-5 as the most popular type of intermittent fasting, and have had people ask me why we don’t like it. To me, the worst feature of Fast-5 is that it encourages you to eat when you are not hungry. That seems a very bad lesson to learn. It is very un-natural, and must have negative consequences — though I’m not aware of it ever having been studies.

In the Fast-5 diet, you have a five hour ‘window’ during which you eat each day. If you have a large meal (i.e. supper) at the start of that time-span, you are probably just beginning to get a little appetite back five hours later. But before the five hours are up you need to eat again, knowing that you will not be able to eat for 19 more hours, so you force yourself to have another (admittedly smaller, but larger than you really want) meal.

Say you follow the exact schedule used in the book, and eat at 5:00 PM. You probably finish around 5:30 or 5:45, depending on the meal. Then, about 9:00 PM, just 3.5 hours after you finished your dinner, you think ‘Oh I better eat now, fasting starts in just another hour!’ — so you make a sandwich or other good-sized mini-meal, and eat it about 9:30, four hours after you finished dinner. You are not really hungry at all, and are just eating because it will be ‘too late’ if you wait until your appetite returns.

As I’ve stated before, that 5:00 PM to 10:00 PM eating schedule is also a poor choice, because you spend all day waiting for ‘feeding time’ and then go to sleep on a full stomach. Much better is to go to sleep just as you are getting hungry again. If your sleep hours are too late in the fast, hunger can make it hard to get to sleep, so you don’t want to go too far in that direction either. Put your sleep hours in the middle of the fast, and you will sleep away some of the most difficult hours, those when your appetite returns.

You may dream of food, but I assure you dreamed food is absolutely non-fattening. You will wake up a bit hungry, but you probably are used to that — most people are a bit hungry in the morning. That feeling will persist until the end of the fast — but it will not become a gnawing pain or severe longing, because you know it is not very long until you will eat again.

The other problem with Fast-5 is that it forces calorie restriction. That is fine if you goal is rapid weight-loss, but it is a short-term means to an end, rather than a satisfying lifestyle choice. The recommendation that you should only fast a couple days a week once you have achieved your ideal weight is not satisfactory, because it unbalances your life. Suddenly you have two days each week that you dread, because they are a break from your norm.

It is easier and more satisfying to fast 23 or 24 hours out of each 48. You are fasting less than the Fast-5 but the fasts are slightly longer, and may be more beneficial for that. I say that purely from conjecture, since nobody has studied 19 hour daily vs 23 or 24 hours of each 48 fasting. I suspect the results would be so similar that a very large study-group would be required to have any statistically meaningful results from such a study. My feeling is that the slightly longer fasts probably have slightly more beneficial effect, and that is negated by the lower frequency, so the two fasting styles even-out about the same. Give me two roughly equivalent choices, and I tend to choose the easier — and from experience Isabel and I say our 23/25 schedule is much easier than Fast-5.

Food affects the brain. Well, duh … why don’t I find that headline surprising. Actually, the full headline (not being so succinct as I am) reads: Scientists Learn How Food Affects The Brain: Omega 3 Especially Important. The study being reported is simply an analysis of the literature, so it summarizes all the preceding studies on the subject — I guess that’s why the results are so unsurprising.

The main points of the report are that we need omega 3 fatty acids, probably more than we typically get in a normal diet. Salmon seems to be the best source for these, though tuna has them to a lesser extent, and even walnuts and kiwi fruit are sources of some omega 3 — but the report notes that particular types of omega 3 are more beneficial than others, such as docosahexaenoic acid, which is abundant in Salmon.

The report also cites the benefits to the brain of folic acid — a supplement that used to be recommended primarily for women who were, or might become, pregnant. Not only is folic acid essential for the proper development of a fetus, it is an important nutriment for efficient brain functioning.

This report also mentions something called brain-derived neurotrophic factor (BDNF) but that seems to be produced in the brain, rather than derived from food. The news report seems to associate BDNF with curcumin, without explicitly stating that a relationship exists. Never the less, curry (which contains high levels of curcumin, or the spice cumin) is also beneficial to brain functioning — whether by stimulating or facilitating BDNF is left to us to conjecture.

Bringing the discussion around to intermittent fasting, the report also states that:

A long-term study that included more than 100 years of birth, death, health and genealogical records for 300 Swedish families in an isolated village showed that an individual’s risk for diabetes and early death increased if his or her paternal grandparents grew up in times of food abundance rather than food shortage.

so that:

Controlled meal-skipping or intermittent caloric restriction might provide health benefits, he said.

Well that is cautious enough, isn’t it? Evidence certainly suggests that intermittent fasting WILL improve brain functioning, along with most of the body’s other systems — with or without caloric restriction. Somehow it is not greatly surprising that it is possible to pass some of that benefit on to your children, but why would it benefit grand-children? And particularly through the paternal line? I’ll have to try to track down the original study mentioned, to see if it can offer any plausible explanation.

We have been on our intermittent fast for four months now, and it is again time to report our weights. You will remember (if you have been following) that last month we reported:

Isabel 61.0 kilos (started at 63.8 … 2.8 kilos lost)

Andrew 95.5 kilos (started at 99.1 … 3.6 kilos lost)

Let me say that Isabel tends to have wider swings in weight than I do — I think it’s one of those girl things — hormones and cycles and what-not. When her weight is up, as it was today, it is usually due to water retention, rather than fat-gain. At least that is what I think from looking at her — and I fancy myself something of an expert at looking at women. OK, most men are expert at that, but I’m just stating my observations. Anyhow, here are our current weights:

Isabel 62.4 kilos (started at 63.8 … 1.4 kilos lost)

Andrew 95.1 kilos (started at 99.1 … 4.0 kilos lost)

I suspect in a couple weeks Isabel will weigh in at 61 kilos again, and I have been fluctuating between 95 and 95.5 for the past month or more. I’m not sure if this is a ‘plateau’ that will give way to further loss, or if we are at the limit of our weight-loss for this diet. Either way it’s fine with me — weight loss was not the motive for taking up this regime. Isabel and I both agree we feel healthier, and while a little more weight loss would be nice, it is by no means necessary. We will continue living this intermittent fasting lifestyle with or without further loss of weight.

Another report today describes mice on regular, calorie restricted and alternate day fasting schedules, with and without resveratrol supplement. That’s the chemical in red wine, grapes and some other foods that has been found so beneficial for health. The report focuses on the resveratrol, so it is hard to say for sure, but it seems to suggest that the alternate-day fasted mice outlived even the calorie restricted ones:

Mice on a high-calorie diet without resveratrol lived the shortest length of time and mice on an every-other-day regimen lived the longest, regardless of resveratrol treatment.

They found resveratrol had several beneficial biological effects, corresponding to improved quality of life in humans, but so far as longevity was concerned, the intermittent fasting effects seemed to outweigh the benefit of resveratrol. So myself, I vote for both. I drink my three glasses of red wine daily — not enough for all the resveratrol we need, but any more would contain too much alcohol. Resveratrol supplements have not yet been proven, but even if they do work, they don’t seem to be sold here in Mexico, at least in any of the health-food stores I’ve found in Guadalajara and Chapala-Ajijic areas. So I’m really glad the intermittent fasting regime was proven more effective than the resveratrol — at least in mice. Who know what human studies (when they are finally ready) will show?

The life-extension effect induced through caloric restriction (CR) or intermittent fasting (IF) has been studied more extensively in animal models than amongst human subjects — people just live too darn long for quick study results. A couple years ago researchers suggested that sirtuins might be responsible for the longevity effect observed in CR and IF.

Then came a study that showed fruit flies lived longer on a calorie restricted regime when Sir2 was absent — the opposite of the expected effect. Sir2 is a sirtuin in fruit flies that corresponds to SirT1 in mammals. Now further research indicates that brain cells from rats react better to oxidative stress when SirT1 is not present, suggesting that elderly brains may be harmed by the presence of SirT1.

Sirutuins like Sir2 and SirT1 play a complex role in metabolism, and their activity can not be clearly categorized as either beneficial nor harmful to longevity. More likely, they have some effect on processes that directly affect lifespan, such as glucose metabolism, antioxidant activity and insulin sensitivity.

Biologists are looking for the ’smoking gun’ (or guns) responsible for aging. It’s probably not the sirtuins, though they do play some role in the process. It can seem disheartening to see a promising line of research lead to a seeming dead-end, but in science negative results can sometimes be as helpful as positive findings, in that it further narrows the field and helps better focus attention on relevant factors.