This post is geared to an elite group of readers: Men on LC (low carb) or VLCK (very low carb/ketogenic) diets who engage in moderate to heavy weightlifting on a regular basis. I’ll go a step further and assume they are concerned about boosting their testosterone levels. Testosterone after all, is a pretty important factor in muscle development.

Prior to any research into this topic, my gut feeling was that restrictive diets – low carb in particular – would have negative consequences for testosterone. The rationale for this line of thinking is that restriction of carbohydrates would signal to the body that hard times we’re being experienced and that reproductive functions should be put on hold until more flush times returned. Since women have a greater energy investment in reproductive functions, I would expect that LC and VLCK diets to have even greater effects on female hormones, but that’s a topic for another time. It’s enough just to consider male sex hormones for now.

Let’s see what the research has to say on this matter.

The top Google search results for low carb testosterone bring up sites run by and geared to “roid boys” and muscle heads (bro scientists) [1,2,3]. And for the record, let me say some of it is damn good and quite informative. For a very succinct, straightforward and slickly presented post on this subject see the article from Testosterone Nation reference above.

Bottom line: it doesn’t look good for testosterone levels with respect to weightlifting while eating LC and VLCK. However, there is a glimmer of hope if the carbs that are allowed, are properly timed.

In a study out of the University of North Carolina, 20 endurance athletes were divided into two groups [4]. One was put on a “low carb diet” the other on a “normal carb diet” and then put on 3 days of intensive training. Blood samples were taken over the course of the experiment and analyzed for free testosterone and cortisol. The low carb group’s diet was only defined as 30% of daily intake, which is not very low carb by most standards and the other group referred to as “control carbohydrate” was 60% of daily intake. I know some would have problems with listing carbs as a % of daily intake and not absolute amounts.

I have other problems with the diet regimens in this study.

The subjects prepared their own meals with suggestions about what to consume and kept a log of their diet. But this highlights why human subjects are difficult beasts to do diet research on. After all, you can’t keep them in a cage and feed them human chow pellets. The best you can do for human diet studies is employ a metabolic ward, but this is expensive and restrictive and as such, can only last for a relatively short study period. I often wonder why not employ prepared packaged meals much like Weight Watchers or Atkins microwave meals.

However, the most egregious is that when the subjects were at the research training facility during the training phase, they were supplemented with Polycose, which consists solely of glucose polymers derived from cornstarch, with 87.5 grams of carbs for the normal carb group. Boost High Protein Drink for the low carb group. Good lord! The ingredients in Boost High Protein Drink in order are water, sugar, corn syrup, milk protein concentrate, vegetable oil, soy protein, vitamins and minerals with 33 grams of carbohydrates, 23 grams coming from simple sugars and 45 grams of protein.

You would think in the one situation where the researchers had some control over carbohydrate intake they would have done a better job. They probably got a good deal on Boost at the local CVS. Here’s an idea: since Polycose is a powder that you mix in water why not supplement the low carb group with whatever was needed with 45g of protein powder in water?

While this study is cited in the some of the roid blogs mentioned above, the results are weak in my opinion. There seems to be a general trend of lower free testosterone in the low carb group but it is not significant. There was a significant increase in cortisol levels in the low carb group, however, 24.1 vs 27.6 ug/dl. The authors resort to some statistical contortions to get a significant result for the free testosterone to cortisol level.

Nevertheless, due to these trends toward differing responses in and between the groups, an analysis of covariance (ANCOVA) was also conducted on the fTC ratio in which the initial resting Pre 1 levels of the ratio for each group were used as covariates. This alternative analysis revealed a significant group by time interaction effect for the fTC ratio change.

The authors strategically place in the abstract the dramatic result of 43% significant reduction in the free testosterone ratio to cortisol in the low carb group, using the aforementioned massaging of the data then presenting it as a percentage. In fact, these are percentages of percentages. See why percentages can be misleading. The absolute numbers are way less impressive 1.53 vs 0.82.

I’m nit-picking this study because it is the one making the most rounds from bloggers who most probably only have an abstract available and only see the 43% reduction number.

I did find it interesting that the researchers proposed using the free testosterone to cortisol ratio as a measure of overtraining. It would be nice to have a quantitative value for overtraining rather than subjective one of some muscle head walking by you at the gym declaring that you’re overtraining.

In another study [5] seven healthy men were first put on a high-carb and then a high-protein diet. I only have the abstract, so have no idea as to the actual composition of carbs of each diet other than total calories and fat content were kept equal in both treatments, however, absolute values are provided for the measured testosterone and cortisol. Testosterone was significantly higher after 10 days on the high carb diet than the protein diet (468 +/- 34 ng/dl) vs (371 +/- 23 ng/dl). Cortisol levels were consistently lower in the high carb group after 10 days (7.74 +/- 0.71 micrograms/dl) vs (10.6 +/- 0.4 micrograms/dl ).

The astute reader will notice besides testosterone, cortisol was measured in these studies. We all have heard of cortisol, “the stress hormone”, from mainstream media and supplement manufacturers hawking their latest “cortisol blockers.”

The research would suggest that low carb diets raise cortisol levels [6]. Cortisol in turn, has negative influence on testosterone and is why it must be discussed [7, 8].

Exercise in general, temporarily raises cortisol and testosterone levels. So the goal of the bodybuilder in his training is optimize for the greatest testosterone and least cortisol release. When glycogen stores in the liver and muscles are depleted during a weightlifting session, cortisol is called upon to breakdown muscle for amino acids to create glucose and glycogen in the liver. So ideally, we want to go into the gym with as much glycogen as possible. This is the rationale behind carb-loading.

Hopefully you see where this is going for LCers and especially VLCKers. Since they’re showing up at the gym with low glycogen from the get go, cortisol will rise earlier and to a higher level during and after training in their bodies.

While most of the research shows only a negative correlation between testosterone and cortisol and not a causative one, there is some evidence to suggest a causative effect [7, 8, 9]. One fascinating piece of research out of The University of Texas at Austin would suggest that cortisol not only affects testosterone levels, but also how we respond to it behaviorally [10]. Think of the ultra-competitive juicer or roid rage. Apparently, cortisol blunts the behavioral effects of testosterone.

The study looked at 57 participants in a one-on-one competition. The cortisol and testosterone levels were looked at before and after competition in both the winners and losers. The losers were given a chance at a rematch if they desired. The losers who had high-testosterone/low-cortisol all agreed to a rematch. Those with a low-testosterone/high-cortisol all declined the offer of a rematch.

The author of the UT fluff piece for the study suggests that this makes sense from an evolutionary perspective. If one is in a fight-or-flight stress situation then there is no time for such things as competitive posturing or mating behavior or in the previous study, returning to the gym. No amount of flexing out or posturing is going to save your ass from a saber-tooth tiger.

One last aspect to look at regarding low carbs and testosterone lies with the brain. The brain is constantly monitoring blood glucose levels through the hypothalamus. There is evidence to suggest that a hormone released from the hypothalamus called Gonadotropin Releasing Hormone (GnRH) is inhibited under low glucose conditions [11]. GnRH, through a cascade of biochemical events, influences the testes to produce testosterone.

Okay, what can LC and VLCK folks do, if anything, from being a stressed-out wimp at the gym?

The author of the post at Testosterone Nation has some excellent strategies. His name is Brad Dieter and here are his suggestions.

• Time your carbs. Low Carbers are allowed some carbs, so eat these prior to your workout. He didn’t say anything about immediately following a workout, but I would recommend consuming some carbs post-workout as well.

• Second, increase your protein content so amino acids can be used for gluconeogenesis to reduce cortisol.

• Third, use MCT oils to provide fuel for your workout and potentially reduce cortisol.

One final note and caution: don’t come away from this with this thinking that more carbs equals more testosterone. Excessive carb intake is associated with low testosterone [12].

Photo Credits (morguefile.com):

• Steak: kconners
• Massage: Yoel
• defeat: marykbaird
• stress: pedrojperez
• weights: cohdra
• winners: GaborfromHungary
• tiger: watchthebirdy
• bread: agathabrown
• pie: alcine

In my posts thus far, there is a character lurking in the wings. This mysterious character comes in the form of a rather simple, nondescript molecule consisting of only four carbons, eight hydrogens and two oxygen atoms. It belongs to a class of chemicals called short chain fatty acids or SCFAs. Oh, and it gives vomit its characteristic smell – gotta love Wikipedia for such facts! Give up? If you guessed butyrate, you would be correct.

This seemingly simple molecule has been shown to have a complex range of actions in “test-tube/Petri plate” and whole organism studies for both humans and mice. It has a wide range of implications for colonic health, glucose and insulin regulation, as well as for weight-loss.

Butyrate is produced in the colon mainly through the bacterial fermentation of non-starch polysaccharides and resistant starch (RS). The production of butyrate will in a large part be dependent on the dietary intake of foods containing fiber, e.g. fruits and vegetables. This may be a concern for those on a low-carb diet since the raw material (fiber) for butyrate production is being restricted.

There are several studies in obese humans showing that fecal butyrate and butyrate-producing bacteria are reduced on low-carb diets [1,2,3]. Why should this be of concern? Well, colonic cells prefer to use butyrate as an energy source. In mice, colonic epithelial cell atrophy can be induced by a no-fiber diet, and to some degree, prevented, by butyrate colonic infusion [4,5]. In other words, adding butyrate via fiber consumption can benefit the cells lining the walls of your colon.

The human studies referenced above involved measuring the butyrate levels of the subjects’ feces. You can feel for the research subjects having the ignominy of being put on a restricted diet and then having to collect their stools in a plastic bag. Not fun. Sympathies also go out to the research assistants tasked with pureeing the stool samples. Not fun x2!

What kept nagging at me was whether fecal butyrate levels were indicative of the actual levels in the colon. After all, given that 95% of the butyrate produced in the colon is absorbed and utilized by the colonic epithelial cells for energy, then very little should appear in the feces. At least one would surmise.

It was very refreshing to find a blog post along this same line of thought. The writer suggests that the reduced butyrate levels in the feces in the low carb situation can just as likely be explained as a greater absorption in the colon. However, unlike in experimental cows where a port can be surgically implanted into the rumen, fecal sampling is the best non-invasive tool for measuring butyrate in humans.

Rich reviewed the movie Food, Inc. awhile back. There is a scene where a researcher is being interviewed next to a cow with just such a port [6]. He reaches into the port and pulls out some of the contents. If I remember correctly, he was trying to associate the emergence of deadly E. coli O157:H7 in cows with corn feeding as opposed to grass-fed cattle. He hypothesized this was due to the unfavorable changes in the gut biome.

Regarding the topic of gut biome, there are certain species of bacteria in the colon that are good at turning fiber and resistant starch into butyrate. These bacteria seem to thrive on such things as inulin, psyllium, RS, and fructo-oligosaccharides. I know that Rich supplements his low carb diet with a glass or two of Metamucil, which contains psyllium husks as its primary soluble fiber ingredient (70% soluble fiber, 30% insoluble fiber). I think that some low carbers are too restrictive and forget that not all plant-based carbs are equal. Some are necessary for gut health and have a very low glycemic index.

Thanks for mentioning my Metamucil supplementation, Rob 😉 I use it primarily to smooth the elimination process. Even with a higher carb diet, it’s still difficult to ingest sufficient soluble fiber to facilitate things and it’s twice as difficult when you’re older. Hence, a fiber supplement to the rescue. I mix a level teaspoon of Metamucil with a scoop of creatine powder prior to cooking breakfast. It’s a refreshing concoction and the orange-flavored (sugar-free variety) provides a tasty vehicle for the flavorless creatine powder. If I’m experiencing benefits beyond smoother elimination such as lowering cholesterol, better glucose control, and healthier and happier gut microbiota, so much the better!

In reviewing studies, both mouse and human, there seems to be no real consistency in the type of carbs or control for type and amount of fiber and resistant starch used for the experimental low-carb regimen other than it limits carbs to around 25g per day. This places such a diet within the ketogenic range.

Butyrate may also be important to the low carber since there is some evidence (mouse and test-tube) that it influences the production of a certain satiety hormone, signaling fullness, as well as a metabolic hormone that lowers blood glucose [7,8].

Much attention, both mainstream and academic, has focused on the role of butyrate on colon cancer.

In the test tube, butyrate is capable of interacting with the colonic cell’s DNA to influence such things as cell division, growth, differentiation, and death. All these have implications for both cancer prevention and promotion. The review article, “Does Butyrate Protect from Colorectal Cancer?” showed mixed results in animal models [9]. One problem with these studies is being able to know whether the butyrate administered managed to get to targeted cells in the colon.

In a mouse model, colitis (inflammation of the colon) was chemically induced and then reduced by giving butyrate enemas. I wonder what a mouse enema looks like. Interestingly, there was a human study conducted in the Netherlands where butyrate enemas were given to patients with colitis. No improvement was noticed [10].

Given that butyrate has the potential to stimulate colon cell proliferation, this can have implications both for repair as well as for uncontrolled growth (cancer).

Since it seems like there is always somebody out there trying to cash in on the latest health craze, I searched for butyrate supplements. Keep in mind that butyrate taken orally wouldn’t make it to the colon. However, if the supplement is enterically coated it might or might not get there, but it would be a necessary prerequisite. It didn’t take long to find some products.

I can envision the day where boutique spas will spring up offering butyrate infusion services: Gisele Bundchen fecal transplants and butyrate enemas all the while sipping super-resistant starch smoothies, anyone? Take a few minutes to watch the video below are a great visualization of the gut microbiome and the action of butyrate, just try to overlook the narrator’s pronunciation of “intestine.”

Photo Credits (via Morguefile.com):

• beans: lisasolonynko
• colombo: Prawny
• bran: dave
• DNA: imelenchon

 

The topic of “gut bacteria” has hit the mainstream media like an outbreak of the Norwalk virus on a Paleo cruise ship. The headlines are screaming that bad gut bacteria are making us fat, insulin resistant and the cause behind metabolic syndrome. Likewise, we are hearing the panacea claims for cultivating good gut bacteria: weight loss, insulin and glucose normalization, reversal of type 2 diabetes, and more. This post will be geared towards those following a low-carb diet and will discuss the practical implications of gut microbiota with respect to weight loss and blood sugar control. A more thorough discussion of this topic can be found at the following reference [1].

The fact that human feces are made up of 55% bacteria (dry mass) should give one pause to reflect on this amazing fact prior to hitting the flush lever [2]. In fact, our lower intestinal tract is teeming with bacteria comprised of a wide variety of species. This is referred to as the gut microbiome, and thanks to modern DNA technology, is being mapped like the human genome [3].

The furor over good and bad gut bacteria comes from mice studies showing that mice implanted with feces from obese mice became obese. This was not the case with fecal specimens from lean donor mice [4]. The bacterial species vary in relative amounts with one type present in a lesser ratio in obese mice. This difference in bacterial ratios has also been found for humans [5]. For simplicity’s sake, we’ll call this either “lean bacteria profile” or “obese bacteria profile.”

Mouse and human studies also suggest that the bacteria profile can be altered through diet and exercise [6]. Simply put, the obese bacteria profile can be changed over time to a lean bacteria profile by a low fat/high plant polysaccharide diet. Likewise, a lean bacteria profile can be changed over time to an obese bacteria profile on a high fat/high sugar Western type diet [7]. In a human study, obese metabolic resistant men receiving a fecal transfer from lean donors didn’t lose weight, but did exhibit increased insulin sensitivity [8]. Despite these findings, I wouldn’t rush out just yet, and get a fecal transplant from a svelte supermodel.

It turns out, that obese bacterial forms that are increased relative to their lean counterparts are efficient at extracting energy from the undigested food matter entering the lower intestinal tract. This extracted energy in the form of short chain fatty acids (SCFA) can then be utilized by the host to pack on pounds [9].

Furthermore, there is speculation that the metabolic byproducts of these bacterial forms can negatively influence the host metabolism causing increases in lipogenesis in the liver, decreases in release of satiety peptides from the intestines, release of inflammatory factors into the bloodstream, just to name a few undesirable consequences. Parasites are notorious for influencing host behavior to ensure their survival and multiplication [10].

I think now would be a good time to take a deep breath. While we have some elegant studies, we’re still left with correlations and a lot of speculation. Always keep in mind that correlation does not necessarily equal causation, unless of course when it does.

Okay, so you’re thinking all I have to do is take a probiotic containing the good bacteria. However, I’ve been going through the contortions of using the term “obese bacteria profile” and “lean bacteria profile” for a reason.

It is the relative ratios of these bacterial types where the difference occurs, not the absolute numbers.

We are also dealing with an ecosystem as complex as a rainforest. And like a rainforest, the gut microbiome could be catastrophically upset by ham-fisted interventions like taking a probiotic. A cursory look at the probiotics on the market reveals that all contain bacteria in the obese profile category.

There is another important link between gut bacteria, obesity, metabolic syndrome, insulin resistance, high fat/high sugar diet and that is… wait for it… inflammation! Certain bacteria produce lipopolysaccharides that are recognized by the immune system resulting in a cascade of inflammatory reactions [11].

In an earlier post, I talked about berberine and its ability to control blood sugar and positively alter insulin signaling. There is some research to suggest that berberine influences the gut microbiome to shift it towards the lean bacterial profile [12]. Other things that have been suggested for changing the gut bacteria profile for the better are glutamine, green and black tea and some polyphenols [13, 14].

What about prebiotics? In other words, “Is there something I can feed my gut bacteria to induce a favorable ratio?”

Again, we’re dealing with a delicate balance. Just like fertilizer runoff into a lake can cause an undesirable algal bloom the situation may exist where it’s possible to “overfeed” the gut microbiota. This condition is apparent to those consuming high amounts of high-fiber foods and experience undesirable side effects. On the flip side, it may be possible to “underfeed.” One study of a high protein/very low-carb (20g) diet suggests negative consequences for gut microbiota and gut health in general [15] as a result of nutrient restriction. Prebiotics deserve their own scrutiny and will be covered in a future post

What about what not to feed your gut biota?

Many of those following a low-carb diet and dieters in general, consume some form of sweetener substitute as part of their regimen (Full Disclaimer: I despise the taste of all sugar substitutes and that includes stevia, sorry Rich). There are studies suggesting that things like aspartame can shift the bacteria profile to that of the obese type [16, 17]. Low carbers are also fond of coconut oil and tout it, among other things, as an antibacterial. What effect it might have, positive, negative or neutral on the gut bacteria profile? I have not seen any scholarly work in this area, but a whole lot of speculation in the blogosphere leans mostly towards the beneficial. There is evidence that saturated fat changes the gut profile for the worse [18].

No worries, Rob. We’ll just have to go our separate ways when it comes to stevia – I put that shizz on everything! I plan to do a series on sugar substitutes along with an in-depth post on stevia. I am interested in what effects it may have on gut bacteria.

The overarching concept that I took way from delving into this topic:

• There is a constant and strong back and forth interaction between the gut and organ systems involved in energy production; e.g. liver, pancreas, visceral fat stores, hypothalamus, skeletal muscle.
• This also holds for the immune system. If any disruption of these feedback loops occurs, it can set in motion a vicious cycle of obesity and insulin resistance. So you can’t expect to try to change your gut profile to a favorable one, yet continue to eat the proverbial Western diet, not exercise or change lifestyles that cause inflammation.
• Maintaining a healthy gut profile should just be one of the several strategies as outlined here on PracticalCarbs.com.

References:

14. Henning, Susanne, et al. “Effect of Green and Black Tea Extracts on Intestinal Microbiota and Body Composition in Mice Fed a High Fat/High Sucrose/Western Diet.” The FASEB Journal 29.1 Supplement (2015): 924-27

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Photo Credits (morguefile.com):

• E coli Petri dish: cielo
• Mouse: xandert
• Dung Beetle by xandert
• Statue: puravida
• Cynomys ludovicianus: FidlerJan

 

 

Resistant starches (RS) seem to have appeared out of nowhere in the popular press along with a lot of fanfare about their health benefits. Resistant starches are nothing new, as they’re found to some degree in all plants. Starch is the plant kingdom’s storage form of glucose and is analogous to glycogen in the animal kingdom. That is why, when digested into glucose, it can lead to the insulin spikes that low-carbers are so eager to avoid.

Resistant starches on the other hand, are forms of the starch that cannot be broken down by the starch-digesting enzyme, amylase, and converted into glucose. Resistant starches, however, can be used by beneficial colon bacteria as an energy source. You can think of RS as fuel for gut bacteria.

Amidst the recent hype on resistant starches, some temperance is in order. Resistant starch consumption may be contraindicated for those with certain digestive disorders such as celiac disease, gluten intolerance, small intestinal bacteria overgrowth, and IBS, to just name a few. Furthermore, the reduction in caloric content may be minimal since the fat substances produced by the gut bacteria can be absorbed and burned as calories, which sort of defeats the purpose [1].

There are actually four types of resistant starches, appropriately named: RS1, RS2, RS3 and RS4. We will focus on only one type here: RS3.

Kitchen Chemistry

Type RS3 is formed by cooking the starch source in water and then allowing it to cool. If you’re so inclined, this provides the unique opportunity to take on the role of playing chemist in the kitchen. It also empowers the low-carb dieter to somewhat reduce the glycemic load of a once in a while pasta, bean, potato or rice dish.

Without going into too much messy scientific detail, when heated in water the two components of starch, amylose and amylopectin, form a gel, that when cooled, realign in a process known as retrogradation. This process turns the starch components into a crystalline form that is resistant to the actions of amylase. It may require several days in the fridge for this transformation to be completed.

It’s all in the cooling

Again, some reservation needs to be applied here. While the resistant starch levels are increased by this process, it might turn out to be only a small portion of the digestible starch. The original very high glycemic index of the starch may be significantly reduced, but it may still wind up being in the high range. Again, how this affects you all depends on your personal tolerance for high GI carbohydrates.

Getting back to our kitchen chemistry experiment, as a test case, I want to focus on maximizing RS3 in a potato salad preparation:

First we’re going to select the small red potato variety since they hold up well to boiling and are low in starch. There is some research to show that cooking the starch with an oil increases RS3 [2].

Lower GI Potato Salad Recipe

Ingredients:

• 4 Red Potatoes
• 8 Tbsp EVOO
• 2 Tbsp Apple Cider Vinegar
• Fresh Rosemary
• Salt, Pepper and Oregano to taste

Directions:

1. Bring large pot of water to a boil
2. Add red potatoes boiling water along with 2 Tbsp EVOO. Boil until soft.
   
3. Dunk potatoes in cold water and allow to cool
4. Slice potatoes (retain skins) into wedges
5. Toss the cubes in 6 Tbsp olive oil, 2 Tbsp apple cider vinegar* and fresh rosemary**
6. Season with sea salt, pepper and oregano
7.  Cool in the fridge for at least three days

*The addition of vinegar to cooled potatoes was found to further decrease the GI index in one study.
**Rosemary has been implicated in lowering the GI of meals.

The long cooling time for the potatoes is because red potatoes are high in amylopectin, and take longer to undergo the retrogradation process than amylose [3].

I use an empty Claussen’s sauerkraut jar to store the potato salad. One study found that boiled potatoes stored in the cold for a day reduced the GI of the potatoes by 43%, however, the GI went from a whopping 168 to a still very high 96. Only the abstract was available, and no mention was made to the type of potato used. An even greater reduction in GI may have been achieved if the potatoes were allowed to cool for a longer period [4].

In the immortal words of the late, great, Julia Child, “Bon appetit!”

Thanks for this post on a timely topic, Rob. I’ve been noticing quite a bit of discussion on RS on some of the low-carb and Paleo blogs. I’m more interested in its effects on gut flora from a prebiotic standpoint rather than as a technique to lower GI. I’m not much of a potato eater, though we enjoy a cool, refreshing potato salad during the summer months. Perhaps you can write a follow up post on gut flora and the basics of pre and probitoics. Here’s an article that appeared in the Washington Post after you wrote this about using the same technique with rice. -Rich

The 2015 Dietary Guidelines Advisory Committee recently issued their 2015 dietary guidelines to the Department of Health and Human Services and the Department of Agriculture. These agencies will then jointly compile these guidelines into a document entitled: Dietary Guidelines for Americans, which will then be promptly overlooked, ignored, and scoffed at by a lot of American consumers. Actually, these guidelines already are.

What seems to be noteworthy about the panel’s current set of recommendations is the warning to limit added sugar. And oh, they’ve backed off on their demonization of fats, however, rather reluctantly and tepidly it seems. They won’t receive any argument from me regarding the warning about avoiding added sugar, but even this revision is long overdue and doesn’t go nearly far enough. It seems more like an acknowledgement or capitulation if you will, to the campaign to remove soft drinks from schools in response to the childhood obesity epidemic that’s plaguing America. Sugar is definitely at the root of a lot of nutritional evil, but where are the warnings regarding refined flour products and the over consumption of starch in the American diet. That stuff converts directly to glucose (sugar) once metabolized. Shouldn’t these nutrients be regarded as a form of “added sugar” as well?

The other big revelation, and the one seeming to get the most attention in the media, is the panel’s revised guidelines regarding fat and the consumption of eggs. The new recommendation for fat consumption starts out fine, but it seems that the dietary poopahs are still driving the car with one foot on the gas and the other on the brakes. They recommend getting most of your dietary fat from unsaturated fat. Their recommendation is to obtain fats from fish, nuts, olive oil and vegetable oils. It’s solid advice up to the point where they recommend vegetable oils—the polyunsaturated fats. This is where I have to smack my head. Aren’t vegetable oils known to be a major cause behind inflammation in the body? And why still all the hate for saturated fat? It seems like the dietary panel is still clinging to the notion that animal fat is not healthy. Perhaps the USDA’s Food Pyramid is still casting its long shadow over things while the American Heart Association is still whispering in their ears about the dangers of saturated fat and heart disease.

At least they appear to have granted a reprieve to the venerable egg, which has been unfairly blamed for raising cholesterol levels and fingered as the culprit in heart disease. This is being touted by the media as a major revelation in the new guidelines, but really, did it need to take this long to tell us that we needn’t worry about our egg consumption? Eggs aren’t dubbed “the perfect food” for nothing and it’s a shame that we’ve been scared into shunning them by our government and the health industry.

Though most people will go about eating the way they always have—either consuming healthy whole foods that include eggs, healthy fats, and limiting sugar and refined grains or doing just the opposite, the ones that may possibly be helped are children. The push to improve the diets of school-age kids is a worthy effort and since they are in the custody of the state between the starting and ending bells, it’s the one shot we have at influencing their life choices. Progress may be glacial, but standing by and doing nothing is not an option. Perhaps with time and a little luck, the nutritional lessons they receive at school will be taken home and shared with the adults that should know better.

The Dietary Panel has quite a few sins to atone for. Their guidelines dating back to the 1980s which resulted in the wretched USDA Food Pyramid is directly responsible for the obesity epidemic in the US and which has now gained solid footholds in many other regions of the world. Foisting the notion that the bulk of our diet should consist of grains in the form of bread, pasta, and sugar-laden cereals is hard to forgive. Fortunately, informed people have long ago decided to ignore the pronouncements and guidelines from this group. The result is slowly improving health in this segment that has chosen to think for itself. It would be nice if the media would stop yipping like a lap dog every time the government declares what’s good for us. Instead of make subtle changes to their guidelines, the USDA and HHS should issue an apology for the harm they have caused their nation.