Apologies for the spotty posting the past month. The gym has been very busy which is great but it has really cut into my writing time. Add some CrossFit related travel, the holidays and some other fun and things have thoroughly ground to a halt!
I want to thank Shaf and Brad for sending some pdf’s I needed. I will link to the abstracts or full text article as available.
Hot topics in nutritional research are the interrelated concepts of meal frequency (intermittent fasting) and caloric restriction. Oddly, there is little debate on the topic of caloric restriction and it’s ability to reduce the frequency of diseases such as diabetes, cancer, Alzheimer’s and a host of other ailments. I say oddly because nutritional “science” seems unable to get out of its own way when ferreting out what does and does not constitute healthy eating. Someday nutrition texts or 101 courses may begin with the premise “…H. Sapiens evolved over the Millennia as Hunter Gatherers utilizing an economic strategy of foraging and food sharing that served our species remarkably well until the advent of agriculture…” Not bloody likely I know but worth a hope!
If you recall, caloric restriction has been shown to slow aging in everything from fruit flies to rodents and primates. This is interesting stuff and it offers enticing potential for extending human life except for the fact that most people cannot cope with the constant hunger that accompanies caloric restriction. Intermittent fasting offers a tool that is perhaps more livable than caloric restriction AND may work better, especially when one maintains a normal body weight and activity level with intermittent fasting.
Recent research looks at a few variables, such as a single meal per day and an alternating schedule of ad libitum eating followed by a day of calorie restriction. Both protocols show promise however there are some blind spots we still need to consider in future research.
The first paper I want to look at studies the effect of 3 meals per day (TMPD) vs. 1 meal per day (OMPD) on glucose regulation while keeping calories and macronutrients the same between the two groups. The findings are somewhat confusing and a bit of a let-down for fans (like me) of intermittent fasting:
Impaired morning glucose tolerance test, Impaired insulin release (insulin resistance) and from a related study I will get to in a moment, increased HDL’s’s and LDL’s’s (no particle size specified) and decreased triglycerides, all in the OMPD folks. One additional confounder is that the OMPD people lost body fat while maintaining their weight, which indicated an increase in fat-free mass. The OMPD protocol appears to improve some elements of insulin sensitivity such as decreased triglycerides, although this is far from clear when we see things like impaired glucose tolerance and sluggish insulin response. The authors cover their bases quite well in the discussion and they mention that one may still be processing the large meal from the previous day when the morning tests are taken, however no one is considering the composition of the meals consumed. This is one of the difficulties of nutrition research in that one must alter as few variables as possible to avoid confounders. This makes ones starting point all the more important. In this situation we find that the macronutrient composition for the two studies are as follows:
The caloric intake was set at ~2364kcal for the OMPD subjects and to decrease the volume of the meal, energy dense (refined) food sources were chosen. So what does this mean in terms of meal size for the OMPD folks?
The study authors wanted to take a standard American diet and compare the TMPD vs. OMPD approach. What we find is a modest decrease in fat mass (14.2 vs. 16.3) and increase in fat free mass in the OMPD vs. TMPD (50.9 vs. 49.4). This is fairly impressive to me considering the subjects consumed a large meal with nearly 300g of dense, refined carbohydrate in addition to a sizable chunk of fat and protein. As I mentioned earlier, the OMPD approach resulted in improved blood lipid markers such as increased HDL and decreased triglycerides, but the ambiguous increase of LDL’s, with no report on the particle size. With the decrease in triglycerides we might assume an increase in LDL particle size and consequently a decrease in atherogenic potential…but that is only a guess without lab verification.
What if macronutrient ratios were shifted towards ancestral levels? What if we saw less mixed meals and divisions along protein/fat meals and carbohydrate only meals, with AVERAGE caloric intake remaining the same? What if carbohydrate sources were not refined? We see marked improvements in blood lipid profiles with a shift towards an ancestral diet (low carb), so it would be interesting to use this as a baseline for future investigations.
Another paper I want to look at studies the effects of one day of ad libitum eating followed by a day of 80% calorie restriction on markers of oxidative stress and asthma in overweight adults. This alternate day caloric restriction (ADCR) approach is interesting for several reasons. We see marked improvements in inflammatory markers, systemic oxidative load, blood lipids, and a decrease in severity and frequency of asthma symptoms. At the end of 8 weeks we see an almost 10% decrease in bodyweight and improvements in subjective reports of hunger. If you recall, alternate day fasts in humans have historically fared poorly due to poor compliance due to the extreme hunger of the subjects. In this case however the small (~300kcal) meal on the CR day appears to be enough to stave off hunger and allow for fairly good compliance.
A few things come to mind when I consider these studies:
1-How much of the difficulty people face on either caloric restriction or intermittent fasting is due to the relatively high amounts of refined carbohydrate and the consequent effects this may have on insulin signaling. In Good Calories, Bad Calories Taubes mentions a study in which the individuals were feed up to 10,000kcals per day, far beyond their caloric needs, yet they remained ravenously hungry. Taubes mentions other studies in which individuals are maintained on low carb, calorie restricted diets with virtually no hunger. This is SUCH in interesting and important point that needs wider airplay.
2-What if we START our investigations with a diet that emulates that of our ancestors, then study the effects of meal spacing or caloric content? I think it’s telling that mild caloric restriction or intermittent fasting can mitigate the effects of a high carb diet, but why not start from a better position? One of the key metabolites studied in the asthma paper above was beta-hydroxy butyrate, a ketone. Ketones appears to confer some advantage both from a perspective of redox potential but also from oxidative stress attenuated via hormesis…why not START with a ketogenic or near ketogenic diet? If intermittent fasting improves insulin sensitivity as it appears to we may be able to alter the range of carbohydrate intake and still maintain therapeutic levels of ketosis. If nothing else one way start at a ketogenic level, add intermittent fasting or caloric restriction, and then titrate carbohydrate up until we see an increase in inflammatory markers and oxidative stress. The list of potential ailments that might benefit from this type of intervention includes cancer, diabetes, Alzheimer’s, Parkinson’s, Huntington’s, asthma, a plethora of autoimmune diseases…we hear barely a whisper about this as a research topic yet therapeutic potential is stunning.