Nurtrion News Quicky: ⤹ Energy Reduction & Metabolic Parameters ⤹ "Macrobiotic Ma-Pi 2" = Diabetes Diet 2.0? Plus: Remember You're Eating Foods, Not Figures

Review suggests: On the SAD American diet only energy restriction saves the average Joes & Janes form diabesity.

Have you ever wondered what actually happens to your body, when you start dieting? I mean on a molecular / signalling protein level? If so, today's "Nutrition News Quicky" is for you, because one of the two studies this quicky is dealing with talks about just that: The type and onset of changes and the realization that Mr. & Mrs. Average Joe on their standard Western diets will gain weight, if they don't subscribe to life-long energy restriction. If you don't like that, it appears as if the "Macrobiotic Ma-Pi 2 Diet" could be a solution - or is this just too good to be true?

Energy Restriction & Metabolic Parameters

With all the hoopla about macronutrient composition, timing, etc. and the realization that the calories in vs. calories out equation is not as simplistic as most dieticians still want to have it, the word "calorie restriction" has gotten quite a bad rep in the Internet health community. 

Table 1 Comparison of the metabolic effects of caloric restriction after a variable period of time on (Soare. ahead of print).

If you take a look at overview of its effects in on body composition, blood glucose, lipids, etc. in Table 1, it does yet become obvious that you must not underestimate what will happen if you simply cut back on calories (based on overview in Soare. ahead of print). As long as the nutrition remains adequate (= you get the necessary micronutrients), eating less will lead to improvements in insulin sensitivity. This in turn triggers a whole cascade of beneficial effects that start with the reduction of fasting blood glucose levels and insulin concentration and end with significant reductions in body fat, type II diabetes rates, blood pressure and chronic inflammation.

Hey Mr. Average Joe, you are going to be fat and sick!

What is quite shocking, is the comparison of overweight dieters to Mr. & Mrs. average in a recent study by Soare et al. (2013).

If you take a look at the data in Table 1 you will see that the "healthy control" group Soare et al. defined in their review of the literature will almost inevitably develop a diffuse combination of obesity-related pathologies we call the "metabolic syndrom". In other words, if Soare's assessment of the situation was correct only the dieters will be able to ward off an insidious increase in body weight, blood glucose, insulin, etc. in the long run.
On a more general note, I would like to point out that these "results" (in a way the assumption that everyone who is not dieting is going to become obese is rather a hypothesis) confirms my personal conviction that the ostensibly paradoxical difference between our bodies' inability to compensate for increased vs. decreased energy intakes is also a result of chronic overnutrition - or, to put it differently: If there is a 20% margin in our daily energy requirements within which our weight would be stable, 90% of the weight stable population of the Western obesity belt is consuming those extra 20%, anyway.

This would not just explain why each and every additional cookie people eat ends up on their hips "instantaneously"; it would also provide us with a simple, yet logical explanation that significant weight loss can only be achieved, if you reduce your dietary intake by >20%... but hey, I am getting side-tracked, here ;-)

⤹ "Macrobiotic Ma-Pi 2" = Diabetes Diet 2.0?

In their very recent, hitherto unpublished review of the effects of diet on type II diabetes a group of scientists from the University Campus Bio Medico conclude:

Battle diabesity w/ supplements

"Many dietary regimens are available for patients with type 2 diabetes to choose from, according to personal taste and cultural tradition. [...] Additional randomized studies, both short-term (to analyze psychological responses) and long-term, could help reduce the multitude of diets currently recommended, and focus on a shorter list of useful regimens." (Kahzrai. ahead of print)

A diet that was not (yet?) on the list Kahzrai et al. are referring to, here is the "Macrobiotic Ma-Pi 2" diet. A pretty funky name for a nutritional intervention the efficacy of which has been tested by Francesco Fallucca, Carmen Porrata, Sara Fallucca and Mario Pianesi in recent experiment. The results of this experiment are about to be published in a future edition of the peer-reviewed scientific journal Diabetes/Metabolism Research and Reviews in 2014 with a telling subtitle:

" Gut microbiota, inflammation, diet, and type 2 diabetes"

In conjunction with the word "macrobiotic" in the name of the diet, it should be obvious that the main idea behind this "new" anti-diabesity diet is to tackle the imbalance of the intestinal microbiota of which more and more scientists (e.g.. Musso. 2011; Qin. 2012) believe that it was the cause not the consequence of development of several human diseases, including obesity and type II diabetes (T2DM). As Kahzrai et al. mention in their abstract,

"[t]he main regulators of the intestinal microbiota are age, ethnicity, the immune system, and diet. A high-fat dietmay induce dysbiosis, which can result in a low-grade inflammatory state, obesity and other metabolic disorders. Adding prebiotics to the diet may reduce inflammation, endotoxaemia, and cytokine levels as well asimproving insulin resistance and glucose tolerance." (Kahzrai. ahead of print)

In their overview of the currently available literature, on the effects the administration of prebiotics such as fermentable dietary fibers has on the production of incretins (~satiety hormones), i.e.

• glucagon-like peptide 1 (GLP-1; fatty acid oxidation, glucose control ↑)  and 
• peptide YY (PYY; anorexigenic = hunger ↓), 

as well as its anti-ghrelin (orexigenic = hunger ↑), they highlight a very recent 21-day, intervention study in patients with T2DM. It is one of only few contemporarily available human studies of which the researchers say that they

"have not given robust results because of their limitations; most randomized controlled trials have been  short-term studies (no more than six months), with small sample sizes ( less than 50 subjects), and have focused on surrogate markers rather than clinical end points". (Kahzrai. ahead of print)

Many of these studies, which confirmed the previously referenced beneficial effects on GLP-1 and PYY have been conducted with pregnant women. These studies were able to show that the frequency of gestational diabetes is significantly reduced by probiotic intervention - immediate downstream effects on the children’s growth rate, on the other hand, were not observed (Luoto. 2010a).

"A unique follow-up study (Luoto. 2010b) has suggested that gut dysbiosis during the first stages of life may be associated with the development of obesity; this study investigated the bifidobacterial numbers in infant fecal samples and showed they were higher in children of normal weight than in overweight infants." (Kahzrai. ahead of print)

Luoto et al.'s follow up study is unfortunately does yet share one of the central limitations 90% of the currently conducted experiments have in common: They did not include all the factors that may be involved in the development of obesity, in particular dietary habits.

Table 2: Macrobiotic Ma-Pi 2 Diet typical composition (Porrata. 2009)

This takes us back to the previously mentioned "recent" series of studies, the results of which have not yet been fully evaluated, yet.

As you can see if you take a look at the typical diet composition of the subjects in the first, prospective trial (Porrata. 2009; see Table 2), the "macrobiotic" intervention was exclusively food based. It was composed of 40–50% whole grains (rice, millet and barley), 30–40% vegetables (carrots, kale, cabbage, broccoli, chicory, onions, red and white radish, parsley),  and 8% legumes (adzuki beans, chickpeas, lentils, black beans), plus gomashio (roasted ground sesame seeds with unrefined sea salt), fermented products (miso, tamari, umeboshi) and seaweeds (kombu, wakame, nori).

Bancha tea (tannin-free green tea) was the main source of liquid. The food intake was measured using the weight method for 7 consecutive days in the 2nd and 4th months of the intervention. The same goes for the compliance with the recommended (100% idiotic) macronutrient composition, according to which the subjects had to consume 15%, 20% and 65% of total energy in form protein, fat and carbohydrates, respectively.

Figure 1: Changes in body composition and glucose & fat metabolism after 6 weeks on Ma-Pi 2 (Porrata. 2009)

If you take a look at the data in Figure 1 there is yet still no debating: The tons of macrobiotic whole foods worked magically - irrespective of the suboptimal protein intake (66g per day, only), the study participants lost tons of fat weight and increased their lean body mass - certainly not bad, if you asked me.

There is yet still one question that needs to be answered: Is this a results of the macrobiotics or a result of the obligatory switch from the Western "convenience" to a whole foods diet that induced these changes? If you asked me, it's the latter. This does not exclude the beneficial influence of an increased macrobiotic content of the diet and corresponding changes in the bacterial make-up of the gut. In the end, this is yet a necessarily result of the enforced revisions the sixteen 60-year old adult type II diabetics who were all treated with insulin made to their food selection.
References:

• Luoto, R., Laitinen, K., Nermes, M., & Isolauri, E. (2010a). Impact of maternal probiotic-supplemented dietary counselling on pregnancy outcome and prenatal and postnatal growth: a double-blind, placebo-controlled study. British journal of nutrition, 103(12), 1792-1799.
• Luoto, R., Kalliomäki, M., Laitinen, K., & Isolauri, E. (2010b). The impact of perinatal probiotic intervention on the development of overweight and obesity: follow-up study from birth to 10 years. International journal of obesity, 34(10), 1531-1537.
• Musso, G., Gambino, R., & Cassader, M. (2011). Interactions between gut microbiota and host metabolism predisposing to obesity and diabetes. Annual review of medicine, 62, 361-380.
• Porrata, C., Sánchez, J., Correa, V., Abuín, A., Hernández-Triana, M., Dacosta-Calheiros, R. V., ... & Pianesi, M. (2009). Ma-Pi 2 Macrobiotic diet intervention in adults with type 2 diabetes mellitus. MEDICC review, 11(4), 29-35.
• Soare A., Weiss E.P., Pozzilli P. (2013) "Benefits of caloric restriction for cardiometabolic health, including type 2 diabetes mellitus risk". Diabetes/Metabolism Research and Reviews [ahead of print]
• Qin, J., Li, Y., Cai, Z., Li, S., Zhu, J., Zhang, F., ... & Yang, H. (2012). A metagenome-wide association study of gut microbiota in type 2 diabetes. Nature, 490(7418), 55-60.