ONLINE DRIVERS MEDIA

Its nice to be lean, but is it really worth ruining your health? I dont think so, but everyone is the architect of his / her own future.

I want to say in advance that youd better not read this article if you belong to the ever-increasing number of carbophobs (people who are afraid of carbohydrates) who have been so indoctrinated by the confusing information on the Internet that they are willing to close their eyes to all objective data.

In view of the fact that you kept reading, I assume that you (a) dont belong to this group of blockheads or are (b) a blockhead who is about to scroll down to the comment section to start raving about how bad carbohydrates are, pointing out that "you just have to eat a ketogenic diet to live happily ever after" - spare me this bullshit, please!
Its scaremongering bullshit like that due to which more and more non-athletes develop what Can Zhao et al. describe in their latest paper in the peer-reviewed scientific Journal of Sport and Health Science as "exercise-associated menstrual dysfunction" aka EAMD (Zhao. 2014).

For those who have read the SuppVersity Athlete Triad Series, its no news that menstrual irregularities and amenorrhea in female athletes is closely linked to the imbalance between energy intake and exercise-associated energy requirement (Williams. 2001). Accordingly Zhao et al. wanted to investigate, ...

"[...]whether carbohydrate supplements can reverse EAMD and protect against exercise-induced impairment in ovary as an important part of HPO axis regulation and rebalances the energy intake and energy expenditure to support the reproductive function" (Zhao. 2014).

Now the bad news is that they did this in rodents. 45 healthy mature 2-month-old female Spraguee Dawley rats, to be precise. This sounds idiotic, but in view of the fact that the experimental procedure required that "subjects" are sacrificed in the course of the study its quite reasonable to use rodents, not ladies.

Figure 1:  Treadmill running schedules show the specific timeline and various treatments of each groups (Zhao. 2014)

Figure 1 shows a graphical overview of the study protocol which involved an identical initial exercise period in the course of which the speed of the treadmill was continuously increased for six weeks.

At the end of this initial 6-week study period, the female rats, the ovary epithelial cells of the rodents showed significant abnormalities. At the end of week 9, the follicular cells of the rodents in group E contained swollen mitochondria with broken cristae.

Similar exercise-induced mitochondrial damages were also observed in the EAMD rats with post-exercise rest. In the rodents in group O and G, however, Zhao et al. observed a significant recovery of exercise-induced mitochondria impairment. They showed significant reduction of swollen endoplasmic reticulum and Golgi complex, and increases in abundant organelles, irrespective of whether they had been fed a 30% glucose or 30% oligosaccharide diet.

Normalization of organ changes and hormones w/out increase in energy intake

In contrast to the previously hinted at prejudices, the addition of simple sugars to the rodent diet did not lead to an increase in energy intake - in spite of the fact that the goal was a 30% increase in energy intake from glucose / oligosaccharide supplements, the total energy intake was not higher than in the non-exercised control group (see Figure 2).

Figure 2: Changes in energy intakes in each group throughout 9 weeks study (Zhao. 2014).

In conjunction with the significant improvement in GnRH, LH, FSH and estrogen its thus more than unlikely that a comparable increase in "sugar" intake in human females would trigger the increase in body fat many women fear so much that they are willing to run around tired and infertile for years, although most of them know that reducing the exercise volume and normalizing their eating behavior would solve the problem once and for all.

Figure 3: Relative levels (% of control) of GnRH, FSH, LH, E2 and Progesterone (P) after 9 weeks (Zhao. 2014)

Interestingly, the saccharide polymers (oligosaccharides), which are also commonly found on the plasma membrane of animal cells, where they can play a role in cell–cell recognition, did a slightly better job than glucose, when it comes to the restoration of normal hormone levels (see Figure 3).
Reference:

• Qiang, Xu, Chao YongLie, and Wan QianBing. "Health benefit application of functional oligosaccharides." Carbohydrate Polymers 77.3 (2009): 435-441. 
• Tomten, S. E., and A. T. Høstmark. "Energy balance in weight stable athletes with and without menstrual disorders." Scandinavian journal of medicine & science in sports 16.2 (2006): 127-133. 
• Williams, Nancy I., et al. "Longitudinal Changes in Reproductive Hormones and Menstrual Cyclicity in Cynomolgus Monkeys during Strenuous Exercise Training: Abrupt Transition to Exercise-Induced Amenorrhea 1." Endocrinology 142.6 (2001): 2381-2389. 
• Zhao, Can, et al. "Effects of carbohydrate supplements on exercise-induced menstrual dysfunction and ovarian subcellular structural changes in rats." Journal of Sport and Health Science (2014).

The advantage of HDL is its stability that reduces the risk of plaque build-up in the intestinal wall, which is clogged by the remnants of oxidized LDL and causes heart disease & co.

First things first: We are not talking about "hard experimental evidence" as you could generate it in a randomized controlled trial in a metabolic ward. The data I am reporting today is from a cohort with 1,566 participants with extensive lipid phenotype data completed the Harvard Standardized Food Frequency Questionnaire to determine their daily micronutrient intake over the past year - an epidemiological study that used stepwise linear regression was used to separately evaluate the effects of dietary covariates on adjusted levels of HDL-C, HDL-2, HDL-3, and apoA1.

Interestingly, this is the first study with a quality data-set that determined the association between specific dietary micronutrients with HDL-C, HDL-2, HDL-3, and apoA1, and how these dietary associations differ across the various measures of HDL - not just one.
To identify the HDL-promoters in the diet, the scientists use demographic and clinical variables in the base model. What they found was that numerous dietary intakes increased total HDL-C variance.
The results of their stepwise linear regression model in Table 1 indicate - probably for some people much surprisingly - that all alcohol intake levels were positively associated with HDL-C.

"In addition, magnesium, folate, and the saturated fat, myristic acid (14:0), were all positively and independently associated with HDL-C. Carbohydrate intake, iron, and % of fat derived from animal sources were each negatively additive for HDL-C." (Kim. 2014)

Similar effects from dietary intakes were observed for HDL-2, of which we know that it is decreased in women with rheumatoid arthritis (Arts. 2012) and individuals with other inflammatory diseases (including metabolic syndrom) and associated with a slightly higher reduction in acute myocardial infarction risk than "regular" HDL in several studies (Salonen. Salonen. 1991; Stampfer. 1991; Buring. 1992; Gaziano. 1993) for all alcohol intakes, magnesium, folate, and myristic acid (14:0), eicosapentaenoic acid (20:5, a ?-3 EPA), all of which were positively and independently associated with HDL-2 levels.

Table 1:  Best-fit model from stepwise linear regression predicting HDL-C levels using dietary intake data (Kim. 2014)

The opposite was the case for arachidonic acid (20:4, an ?-6 ARA), carbohydrate and iron intakes, which were both negatively associated with HDL-2 (see Table 1).

Dont forget to put things into perspective!

And just to make sure, I dont get angry emails from bulletproof coffee drinkers: Your coffee is fine, the content of the only "good" saturated fat, i.e. myristic acid, happens to be especially high coconut oil (41%; Sodamade. 2013) and relatively high in butter (12% independent of whether its grass-fed or not; Couvreur. 2006) - surprised? Not really, I guess. As a SuppVersity reader you are by now aware that the bad reputation coconut oil and butter have for being mostly saturated fats is no longer supported by contemporary scientific evidence (Dias. 2014).

And with respect to the total animal fat intake - for the average Westerner thats a good measure of how much processed meat he / she eats, so I would not overrate the small negative association (1/80 of the one of having a ton of carbohydrates in your diet!) the scientists found in the study at hand.
References:

• Arts, Elke, et al. "High-density lipoprotein cholesterol subfractions HDL2 and HDL3 are reduced in women with rheumatoid arthritis and may augment the cardiovascular risk of women with RA: a cross-sectional study." Arthritis Res Ther 14.3 (2012): R116.
• Buring, J. E., et al. "Decreased HDL2 and HDL3 cholesterol, Apo AI and Apo A-II, and increased risk of myocardial infarction." Circulation 85.1 (1992): 22-29.
• Couvreur, S., et al. "The linear relationship between the proportion of fresh grass in the cow diet, milk fatty acid composition, and butter properties." Journal of dairy science 89.6 (2006): 1956-1969.
• Dias, C. B., et al. "Saturated fat consumption may not be the main cause of increased blood lipid levels." Medical hypotheses 82.2 (2014): 187-195.
• Gaziano, J. Michael, et al. "Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction." New England Journal of Medicine 329.25 (1993): 1829-1834. 
• Kim et al. "Effects of dietary components on high-density lipoprotein measures in a cohort of 1,566 participants." Nutrition & Metabolism 2014, 11:44.
• Leon, ARTHUR S., and OTTO A. Sanchez. "Response of blood lipids to exercise training alone or combined with dietary intervention." Medicine and science in sports and exercise 33.6 Suppl (2001): S502-15.
• Salonen, Jukka T., et al. "HDL, HDL2, and HDL3 subfractions, and the risk of acute myocardial infarction. A prospective population study in eastern Finnish men." Circulation 84.1 (1991): 129-139. 
• Sodamade, A¹, and O. S. Bolaji. "Fatty acids composition of three different vegetable oils (soybean oil, groundnut oil and coconut oil) by high-performance liquid chromatography." Chemistry and Materials Research 3.7 (2013): 26-29.
• Stampfer, Meir J., et al. "A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction." New England Journal of Medicine 325.6 (1991): 373-381.