Showing posts with label diets. Show all posts
Showing posts with label diets. Show all posts
Friday, March 11, 2016
Scientists Probe the Interaction Between Saturated and Unsaturated High Fat Diets and Their Corresponding Carbohydrate Sources Cornstarch vs Fructose
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| This add is a perfect example of how saturated fat, in this case lard has always been blamed for the "lard" on ones hips. |
With the publication of the data of a their latest rodent study, the scientists have already taken the first step to a new, an "interactionist" perspective on the obesogenic effects of saturated vs.unsaturated and simple vs.complex carbohydrates and their interaction with another previously overlooked factor that has gotten quite some attention in the past months: The gut and its inhabitants.
Goodbye! Nutritional scapegoatism
It goes without saying that this model study is nothing but a first step on a long road we still have to travel, but the differential effects the four diets (see Table 1)...
the soybean powered high cornstarch diet (OS),
Table 1: Composition of the diets. - the lard-laden high cornstarch diet (LS),
- the soybean-powered high fructose diet (OF), and
- the lard-laden high fructose diet (LF)
World premiere! I know it sounds hilarious, but this is actually the first study I have seen that focused on nutrient interactions, instead of individual (macro-)nutrients in diets that are not even suitable to isolate the effects of the nutrient of interest - most prominent example the "high fat diet" which is high in fat (45% of the energy is the standard; there are yet also "high fat" diets with only 32% of the total energy from fat; Gajda. 2008) but leaves enough room for carbohydrates to complement, some would say "trigger" the obesogenic effects by providing a pro-insulinogenic stimulus that will blunt the oxidation of the dietary fat and help drive it into the cells.
If you take a closer look at the actual study outcomes, you will see that the answer(s) the study provides are about as complex as its design.In contrast to the dietary fat which had no independent effect on any of the measured markers of gut function, the carbohydrate source, i.e. cornstarch vs. fructose lead to significant differences in total small intestinal mass, mean pH of the ileal digesta and the mucosal activity of sucrase, all of which were increase on the high fructose diet.
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| Figure 1: Serum lipid levels of the rodents after 4 weeks on obesogenic diets containing different forms of dietary fat and carbohydrate (Jurgo?ski. 2014) |
"Both the dietary fats and carbohydrates contributed to changes in the total SCFA concentration in the caecal digesta of rats (p < 0.05 and < 0 0.001, respectively). The highest total SCFA concentration was in group LS, while group OS had a significantly lower concentration (p ?0.05). Similarly, the acetate concentration in the caecal digesta was influenced both by dietary fats and carbohydrates (p < 0.05 and p < 0.001, respectively) with a similar span of differences among particular groups (p ?0.05). The type of dietary carbohydrate had significant influence on the propionate and isobutyrate concentrations in the caecal digesta (p < 0.001 and p < 0.05, respectively); however, both dietary factors had an interactive effect on their concentrations (p < 0.05). The highest propionate concentration was observed in the LS and OS group, whereas significantly lower concentration was found in the OF group. The lowest isobutyrate concentration was in group OF and it was significantly higher in group OS (p ?0.05)." (Jurgo?ski. 2014)The serum lipid profiles were influenced by both, the types of fats and carbohydrates as shown in Figure 1. Whats particularly striking, here, is the nasty effects of a combined lard + fructose feeding on the triglyceride levels.
A similar fat-dependence as for the fructose induced triglyceride boost can be observed for the levels of total and HDL cholesterol, which were increased only by the combination of fructose + saturated fat. In the rodents that received soybean oil with their coke, ... ah, I mean with their fructose, the researchers observed the exact opposite trend and a 5x lower yet similarly increased artherosclerosis risk (as evidenced by the 5x higher atherogenic index).
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| Suppversity Suggested Read: "EGGS - A Four-Letter Food Improves Both Cholesterol Particle & Phospholipid Profile + HDL-Driven Lipid Reverse-Transport" | read more |
Yes, I know - thats only rodent data, there is no information on body weight, or the gut microbiome and even the impact on glucose metabolism wasnt measured (you can predict from the triglyceride levels, though, that the animals lard + fructose diet had the lowest insulin sensitivity), the reason I still spent a whole article on this paper is that this is the kind of study, wed need if we actually want to understand "why we are fat" from the inexplicably popular (macro-)nutrient perspective... I mean, lets be honest: On the level of food items, the complexity is not a problem and we all know the food items that propel the obesity epidemic, dont we?
- Gajda, Angela M. "High fat diets for diet-induced obesity models." A Report for Open Source Diets (2008).
Friday, January 8, 2016
High Protein Diets Acid Load Calcium Loss Osteoporosis and a 50 Increase in Diabetes Risk Is There a Link
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| Shouldnt it be obvious that the "happy medium" must be the solution, when high protein leads to brittle bones, and low protein to frail muscle? Sure! But where is this "happy medium"? |
Another paper (Cao. 2014), Jose Antonio, the CEO of the ISSN and the editor of the ISSNs journal posted on Facebook yesterday, didnt get as much media attention, though.
No wonder, the message of this study is after all not in line with one of the fundamental arguments you will hear, whenever you question the allegedly necessary restriction of total protein intake to 0.8g/kg, maximally 1.2g/kg protein per kilogram body weight day in the current nutritional guidelines:
"[...S]hort-term consumption of high-protein diets does not disrupt calcium homeostasis and is not detrimental to skeletal integrity."
Thats not what you will learn at med-school and it is certainly not in line with the hysteria about protein intakes that are 2x or even 3x higher than the 0.8g protein per kilogram body weight we are supposed to consume. Apropos RDA, the subjects in the control group of the said study by Jay J Cao et al. consumed a diet that contained exactly those 0.8g/kg body weight thats supposed to be good for us. The 21 human guinea pigs in the treatment groups, on the other hand, consumed 2x and 3x more than the average dietitian would recommend and they did so for 31 days (Cao. 2014).
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| Figure 1: Protein intake (in g/day; left), mineral intake (in mg/day; middle) and calculated renal acid load (in mEq; right) of 49 normal weight, healthy men (n=32) and women (n=7) who consumed normal (0.8g/day), high (1.6g/kg per day) and very high protein (2.4g/kg per day) energy restricted (40%) diets for 4 weeks (Cao 2014) |
Equations vs. experiments | PRAL vs. urinary calclium loss | theory vs. practive
The urinary analysis the scientists conducted does yet speak a very different language. There is, as the scientists emphasize in the discussion of the results no evidence that
In that I would like to emphasis the importance of adequate calcium (min. 800mg/day) and vitamin D intakes (800-1000IU/day) and the fallacy of the word "habitual". The study at hand did not test the effects of "habitual" high protein consumption. It tested the effects of short-term (28 days) high protein consumption in a low calorie scenario, which is by definition less prone to produce adverse inflammatory and thus potentially pro-osteoporotic side effects (Mundy. 2007)."habitual consumption of dietary protein at levels above the RDA [would] significantly alter urinary calcium excretion, dietary calcium retention, or markers of bone turnover or BMD, despite increased urinary acidity. These results indicate that diets that are 2 or 3 times the RDA for protein are not detrimental to calcium homeostasis when calcium and vitamin D are consumed at recommended intake"
Suppversity Suggested Read: "High protein diet = high protein loss" | more
Not eating enough protein could increase bone loss, when youre dieting
In view of the fact that the evidence I am about to cite, stems from rodent model of postmenopausal bone metabolism, I deliberately used the word could in the headline of this paragraph. And still, the way in which the low protein diet "negatively impacted bone mass and magnified the detrimental effects of vitD and/or estrogen deficiencies" (Marotte. 2013) in the pertinent study from the Buenos Aires University is particularly disturbing.
High dietary acid load increases diabetes risk by more than 50%: In spite of the fact that this is neither bone- nor kidney-specific, the 56% increase in diabetes risk scientists from the Gustave Roussy Institute in France report in their latest paper in Diabetology, for the 16,621 subjects with PRAL values of only 7 mEq/day is so impressive that I simply had to include it in this article. Specifically in view of the fact that a brief glimpse at the food intake of the subjects in the figure to the left will suffice to see that protein is by no means the only "acid" offender in the SAD diet.
The (postmenopausal) women the scientists try to model with their ovariectomized rats (=rats whose ovaries have been removes) are after all one of the many patient groups who are advised to carefully control their protein intake to make sure that the additional acid load will not compromise their bone health even further and that in spite of the fact that there is ample evidence that the current RDA for protein is inadequate to maintain optimal health, particularly when the total energy intake is restricted and especially in populations who are susceptible to bone loss (Kerstetter. 2005; Chernoff. 2004). |
| Figure 2: We know for quite some time not that low protein diets decrease the absorp- tion of protein (Kerstteter. 2005). Its not certain if this is "just" a homeastatic me- chanism to stabilize the net/acid balance. |
In their 2005 study, Kerstetter et al. were in fact able to show that protein intakes that are 2.6x higher than the RDA increase the effective absorption of calcium from the diet (see Figure 2).
This increase stands in contrast to the significant decrease in calcium absorption the researchers observed in the healthy young (age: 26y) women in the low protein arm (0.7g protein per kg body weight) of the study and should remind us that a reduction in protein intake is not going to stop the insidious loss of bone thats caused by the triage of low estrogen, no exercise and a diet that may be low in protein, but high in acid producing grains (Remer. 1995) and devoid of alkaline fruit and vegetables.
I could now go more into details, but I will just leave you with the notion that the "paleo diet" is, despite its high meat content, among the most kidney-, and above all bone-friendly diets we know. In fact, its fruit and vegetables content yield a net alkaline renal load, and will lead to significant improvements in urinary calcium excretion rates (Appelet. 1997; Frassetto. 2013).
? Note: If you want more about the "Paleo connection" - let me know this (best on Facebook) and what you would be most interested in and I will address that in a future SuppVersity article.
Practically speaking: The results of the Cao study tell us that you can get away with a high protein load in otherwise SAD-ly (SAD = standard American diet) normal diet in the short run. What it does not tell you is that you can keep on this kind of "just add a ton of protein to the regular junk you eat diet" with ever-increasing dietary acid loads wont hurt your kidneys, bones and pancreas (see red box) in the long run.
If you want to eat a high protein diet, thats free of kidney, bone, or general meta- bolic side effects, it will thus have to have the fruit and vegetable content of what we currently deem a "paleo diet" - a diet with a relatively high protein content, tons of vege- tables, tubers and fruit and a limited (not no!) amount of grains. This will bring your citrate, magnesium and potas- sium intake up spare calcium and help you to ward off the evermore prevalent diabesity epidemic.
Bottom line: It may be human, but still is idiotic to isolate any single macronutrient as "the reason" for osteoporosis and bone loss. Looking exclusively at what we could potentially be doing wrong is not going to help us here. Rather than that, we should look at what we can be doing right - in other words, what should we eat, if we want to maintain not just bone-, kindey-health, but also muscle- and metabolic health (note: protein alone wont help you maintain muscle mass).
If we look at the results of the previously referenced trial by Frasetto et al., in which the researchers from the University of California San Francisco, which achieved a reduction of the potential renal acid load from 28mEq (which is more than the PRAL of 7mEq thats associated with a >50% diabetes risk; see red box) to -96 mEq on a diets that differed not in macronutrient, but in food, and consequently micronutrient-, specifically mineral-content, you will be hard pressed to keep the deabte on the short-sighted "carbohydrates are good, protein is bad and fat is the devil, anyways"-level it is currently on.
We should be talking about food, instead. Not just about "more fruit and vegetables", but also about what you will necessarily have to skip for them, if you want your diet to work: Highly processed foods, including meats(!), sodas and other sweetened drinks, white bread, candy, chips, etc. Its not that you cant ever eat any of those, but as long as any of these items is on your list of foods you eat on a daily basis, there is still room for improvement.
If we look at the results of the previously referenced trial by Frasetto et al., in which the researchers from the University of California San Francisco, which achieved a reduction of the potential renal acid load from 28mEq (which is more than the PRAL of 7mEq thats associated with a >50% diabetes risk; see red box) to -96 mEq on a diets that differed not in macronutrient, but in food, and consequently micronutrient-, specifically mineral-content, you will be hard pressed to keep the deabte on the short-sighted "carbohydrates are good, protein is bad and fat is the devil, anyways"-level it is currently on.
We should be talking about food, instead. Not just about "more fruit and vegetables", but also about what you will necessarily have to skip for them, if you want your diet to work: Highly processed foods, including meats(!), sodas and other sweetened drinks, white bread, candy, chips, etc. Its not that you cant ever eat any of those, but as long as any of these items is on your list of foods you eat on a daily basis, there is still room for improvement.
References
- Aparicio, V. A., et al. "High-protein diets and renal status in rats." Nutrición hospitalaria: Organo oficial de la Sociedad española de nutrición parenteral y enteral 28.1 (2013): 232-237.
- Appel, Lawrence J., et al. "A clinical trial of the effects of dietary patterns on blood pressure." New England Journal of Medicine 336.16 (1997): 1117-1124.
- Cao, Jay J., et al. "Calcium homeostasis and bone metabolic responses to high-protein diets during energy deficit in healthy young adults: a randomized controlled trial." The American journal of clinical nutrition 99.2 (2014): 400-407.
- Chernoff, Ronni. "Protein and older adults." Journal of the American College of Nutrition 23.sup6 (2004): 627S-630S.
- Frassetto, L. A., et al. "Established dietary estimates of net acid production do not predict measured net acid excretion in patients with Type 2 diabetes on Paleolithic–Hunter–Gatherer-type diets." European journal of clinical nutrition 67.9 (2013): 899-903.
- Kerstetter, Jane E., et al. "The impact of dietary protein on calcium absorption and kinetic measures of bone turnover in women." Journal of Clinical Endocrinology & Metabolism 90.1 (2005): 26-31.
- Mundy, Gregory R. "Osteoporosis and inflammation." Nutrition reviews 65.s3 (2007): S147-S151.
- Remer, Thomas, and Friedrich Manz. "Potential renal acid load of foods and its influence on urine pH." Journal of the American Dietetic Association 95.7 (1995): 791-797.
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