Now let’s talk about science even thought the carnivore zealots don’t believe in science. Is it eating only meat that contributes to good health or is it eating high fats? We know what high fat diets do because there is tons of research, but there is nothing on protein only diets. So we can't just make assumptions. Now, just a word on the high fat diets, even these guys admit eating vegies is a good thing as fat and protein can’t supply the much needed nutrients.
Volek JS, Phinney SD, Forsythe CE, Quann EE, Wood RJ, Puglisi MJ, Kraemer WJ, Bibus DM, Fernandez ML, Feinman RD.
Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids. 2009 Apr;44(4):297-309. doi: 10.1007/s11745-008-3274-2. Epub 2008 Dec 12. PMID: 19082851.
Abstract
We recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (approximately 1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat
rotein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (-12%) and insulin (-50%) concentrations, insulin sensitivity (-55%), weight loss (-10%), decreased adiposity (-14%), and more favorable triacylglycerol (TAG) (-51%), HDL-C (13%) and total cholesterol/HDL-C ratio (-14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial lipemia (-47%), the Apo B/Apo A-1 ratio (-16%), and LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (-20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.
So two hypocaloric diets were compared:
- Low carb (12% carb, 59% fat, 28% protein)
- Low fat (56% carb; 24% fat, 20% protein.
Yet despite this considerably greater intake of saturated fat, the low-carb dieters reduced both their number of small, dense LDL cholesterol and their HDL/LDL ratio to a greater degree than those who ate a low-fat diet. In addition, triglycerides decreased by 51 percent in the low-carb group--compared with 19 percent in the low-fat group. Seems it was discovered that LDL is divided into 2 sub-fractions: small density LDL- B and large density LDL-A. Studies show that people whose LDL particles are predominantly small and dense, have a threefold greater risk of coronary heart disease. Furthermore, the large and fluffy type of LDL may be protective. Lipid EXPERT, Dr. Ron Krauss found that when people replace the carbohydrates in their diet with fat--saturated (SFA) or unsaturated (PUFAs) -- the number of small, dense LDL particles decreases. Small dense LDL particles permeate the endothelial cells and gain access to the wall of the artery where they cause damage leading to plaque. The large particles are not able to penetrate the cell wall and instead cause HLD levels to rise. Over a decade ago researchers reported that men with the highest number of small, dense LDL sub-fractions had four times the risk of developing clogged arteries than those with the fewest. Yet they found no such association for the large, fluffy particles. Further research has shown that by simply reducing the carbs in your diet (starches/sugar) you can decrease the LDL small particles and increase the LDL large particles. PROTEIN intake seems to have little to do with this as both diets had 28/20% protein.
According to author Jeff Volek, Ph.D., R.D., two factors influence the amount of fat coursing through your veins. The first, of course, is the amount of fat you eat. But the more important factor is less obvious. Turns out, your body makes fat from carbohydrates. It works like this: The carbs you eat (particularly starches and sugar) are absorbed into your bloodstream as sugar. As your carb intake rises, so does your blood sugar. This causes your body to release the hormone insulin. Insulin's job is to return your blood sugar to normal, but it also signals your body to store fat. As a result, your liver starts converting excess blood sugar to triglycerides, or fat.
Now to bodybuilders……..type II muscle fibers are very much glycogen dependent. Which is why most bodybuilders tailor their carb intake to before training and after. Only to have the glycogen stores for a hard workout and to replace the stores after training. Too much carbohydrate spills over and converts to triglyceride and also stores as fat. It is rare to find a competitive bodybuilder that goes zero carb, even the last two weeks.
In Volek's study the subjects on the low carb diet had a greater loss of fat in their blood. Which means their cholesterol levels dropped significantly. Restricting carbs keeps insulin levels low, which lowers your internal production of fat and allows more of the fat you do eat to be burned for energy. In the above study, subjects eating the low carb diet reduced cholesterol, triglycerides and lowered insulin.