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The Truth About Carb and Fat Blockers

The Truth About Carb and Fat Blockers

Imagine eating all the “naughty”, guilty pleasure foods (pies, doughnuts, french fries, etc.) you want, yet never having to deal with the unsightly weight gain or awful bloated feeling that accompanies these epic binges all because you took a pill.

It’s the stuff of dreams.

As it turns out such things do exist, or at least, that’s what marketers would lead you to believe.

Related - Carbs are Not the Enemy

These “magical”, quick-fix weight loss aids are known as carb and fat blockers, and they’re yet another fad in the long line supplements designed to combat our ability to exercise any modicum of control over our gluttonous desires.

Today, we’re going to learn the truth about carb and fat blockers -- what they do, how they work, and do they really prevent your body from digesting all of the nutrients.

What are Carb and Fat Blockers?

Carb and fat blockers are a subcategory of the fat burner niche dedicated to reducing calorie absorption from the two most troublesome macronutrients -- carbohydrates and fats, respectively.

Basically, these compounds prevent or reduce the amount of carbohydrates and fats your body absorbs from the food you eat.

Yes, such things do exist, and, in fact, they have been studied (not extensively, mind you). Furthermore, they even appear to work in some capacity, but let’s not get ahead of ourselves.

First, we need to discuss how they work.

How Do Carb and Fat Blockers Work?

Carb and fat blockers tend to work primarily in one of two ways:

Direct Inhibition

The nutrient blocker will find a carb or fat molecule and bind to it. When the nutrient blocker “connects” to its target molecule, the body cannot absorb it -- meaning you cannot obtain energy (calories) from it.

When dealing with over-the-counter dietary supplements, direct inhibition isn’t really employed all that much as most companies don’t want to prevent the vitamin absorption that accompanies direct inhibition, they just want to sell you on the idea of blocking the absorption of carbohydrates and fats. And, that brings us to the second means by which carb and fat blockers work...

Indirect Inhibition

In order to properly digest and absorb nutrients, the body requires enzymes to properly break apart the bigger macronutrient molecules into smaller, “easier” to work with pieces. Carb and fat blockers sometimes target these enzymes and bind to them (known as enzymatic inhibition), rendering them inert and unable to support the digestion process.

FYI, most carb and fat blockers that you will find on the supplement store shelf work via enzymatic inhibition. This is primarily due to the fact that carbs and fat rely on a collection of different enzymes to be digested properly. And, for those of you who forget some of your early biology classes, enzymes are proteins that help catalyze reactions, which in this case is the metabolism of nutrients.

The Role of Enzymes in Digestion and Nutrient Absorption

To understand the role enzymes play in the digestion and nutrient absorption process, let’s look at the digestion of carbohydrates in the body as an example.

After powering down some pizza, potatoes, or popcorn (or whatever other form you choose for your carb indulgence), the available carbohydrates (polysaccharides) in those foods are α-linked sugar units that are initially broken down into oligosaccharides or disaccharides by the enzyme amylase in saliva or the pancreas. (α-amylase hydrolyzes the α-bonds of large α-linked polysaccharides.) [1] Note that only about 5% of the breakdown of carbohydrates occurs in the mouth. [6]

Now, it’s important to note that only monosaccharides (glucose, fructose, and galactose) can enter into the bloodstream and be utilized by human body. Therefore, in order for our body to get an energy from these carbohydrates, they must be further broken down, which is where our next enzyme comes into play.

Oligosaccharides and disaccharides are hydrolyzed in the small intestine to monosaccharides, such as glucose and fructose, by α-glucosidase, a brush border enzyme that is secreted from epithelial cells in the intestine. [2]

The final step in carbohydrate digestion involves α-Glucosidase acting on the α(1→4) bonds breaking starches and disaccharides into glucose. [3,4]

Inhibiting this enzyme can reduce carbohydrate uptake and subsequently reduce after-meal blood sugar, making it particularly intriguing for Type 2 Diabetes researchers. [5] Since less glucose is absorbed, as a result of incomplete carbohydrate digestion, blood glucose levels could be reduced long-term, leading to a small reduction in hemoglobin A1c (HbA1c) levels. [6]

Researchers have identified α-glucosidase inhibitors in plants, some of which have shown promise. We’ll get to those in a bit, but first, what happens to the carbohydrates that aren’t completely broken down?

Where do the undigested carbohydrates go?

Carbohydrates that cannot be, or are resistant, to digestion by the enzymes of the small intestine enter the colon. There, they are fermented by your gut bacteria to produce short-chain fatty acids (such as butyrate), carbon dioxide and methane (gas). [5]

And it’s here we start to see some of the potential issues with carb and fat blockers, carb blockers in particular -- they can lead to a lot of cramping, flatulence, and even diarrhea. White kidney bean (Phase 2) in particular has been noted to have these side effects. [8]

Granted, researchers state that these effects eventually subsided with continued use of the product, but this begs the question that if something is causing you distress, wouldn’t it be easier to just reduce the amount of carbohydrates you eat and not have to bother with the carb blocker (and subsequent fart maker) in the first place?

With that taken care of, now let’s see what the research has to say as to the true effectiveness of these carb and fat blockers. Do they actually prevent your body from absorbing any significant amount of calories?

Carb and Fat Blocker Research

Several drugs have been developed targeting various carbohydrate hydrolyzing enzymes; however, researchers have stated that diabetic patients can develop resistance to these pharmaceuticals. As a result researchers have searched extensively for α-amylase and α-glucosidase inhibitors from natural sources in the hopes that they would bring greater promise for long-term success.

One of the most well-known carb blockers is white kidney bean extract, derived from Phaseolus vulgaris. Chances are you’ve come across this one before in your search for the best fat burners under the brand name “Phase 2”, as it was one of the earliest natural carbohydrate inhibitor backed by several research trials.

Phase 2 (White Kidney Bean Extract)

Phase 2 works by blocking the α-amylase enzyme, which as we explain above, prevents some starch digestion.[9] Remember, only about 5% of total carb digestion occurs in the mouth due to amylase, so that still leaves A LOT of carbohydrate that your body can digest and absorb.

Studies using Phase 2 have noted it can help weight loss when it’s used alongside a high carb diet. [10,11,12] However, other studies have noted that:

“no significant changes from baseline in hip circumference, triglycerides, fasting glucose, total cholesterol, appetite control, hunger, energy level, and percent body fat, neither were there any significant differences between groups.” [10]

Meaning that kidney bean had no significant impact on meaningful weight loss despite reducing some of the carbohydrate uptake.

Additionally, most of these studies are confounded by the fact that the manufacturers of the supplement funded most of them. While this isn’t always a concern with supplement studies, the fact that there’s not much independent evidence demonstrating the efficacy of white kidney bean is suspect.

Salacia reticulata

Salacia reticulata is an intriguing carb blocker known to block multiple carbohydrate digestion enzymes in the body, including sucrase, maltase, and isomaltase.

How is this possible?

Salacia reticulata is rich in salacinol and neo salacinol, two compounds that have been documented to be slightly less potent than acarbose -- a prominent pharmaceutical carb. [13,14]

Rat studies have noted that salacia reticulata can decrease glucose absorption.[15] And, human studies (using both diabetics and healthy individuals) note that its effective for reducing insulin secretion and glucose absorption. [16,17,18]

As a result, researchers note that it may be useful for managing prediabetes as well as kidney disease. However, this still doesn’t negate the fact that you could accomplish the exact same benefit by simply lowering your carb intake.

Ɑ-Cyclodextrin

α-Cyclodextrin is a soluble dietary fiber derived from corn, and can be found in supplements under the name FBCx®. [26] Researchers believe that it can form a stable fat–fiber complex in the stomach and can resist the actions of pancreatic lipases, meaning it prevents fat digestion.

As the fat-fiber complex passes into the large bowel, it seems to resist fermentation by gut bacteria, in effect sidestepping the flatulence and explosive diarrhea of other notable carb and fat blockers.

Studies on α-Cyclodextrin show promise that it can successfully reduce postprandial glucose levels as well as fat absorption from a meal. [26,27,28]

However, it does not COMPLETELY reduce glucose or fat digestion, meaning your body will still digest and absorb some of the carbohydrates and fats from the meal you eat containing α-Cyclodextrin.

Furthermore, these reductions in carb and fat uptake occur in a dose-dependent manner, and when dosed up to 5-10 grams (the dose needed to get real effects), test subjects report experiencing GI distress similar to other carb and fat blockers.

Additional Research on Carb Blockers

As we’ve stated several times in this piece, carb blockers inhibit enzymes needed for the digestion of carbohydrates, but they don’t block all of them. Research indicates that at bat, carb blockers inhibit 50–65% of carb-digesting enzymes. [20]

Now, it’s worth noting that just because 50 or 60% of the enzymes are blocked, does NOT mean that 50 or 60% of the carbohydrates you eat alongside your carb blocker will be blocked.

In fact, one study documented that while an alpha amylase inhibitor blocked 97% of the enzymes, it only prevented 7% of the carbohydrates from being absorbed. [21]

This is most likely why studies using carb blockers often find no significant difference in weight loss between those who take the supplements and those who don’t. [10,22]

And, in the studies where subjects using carb blockers did lose weight, average weight loss was only 2-5 pounds more than the control group. That’s hardly a significant amount of weight loss in the grand scheme of things, especially when you consider the amount of people that are overweight and obese in society.

It’s also worth mentioning that these products are only effective when eating a high amount of carbohydrates. Therefore, if you simply reduce total carbohydrate intake, there is no need for these quasi-effective supplements.

Now, one thing that is interesting, and worth discussing while we’re on the subject of carb and fat blockers is that there is some evidence using these supplements may help reduce appetite.

More specifically, the phytohaemagglutinin contained in carb blockers has been shown to significantly reduce food intake. In animal studies (i.e. rats), those those administered the compound consumed 25-90% less. [23]

However, this effect was short-lived, with tolerance setting in, and the rats ultimately eating as much as they did initially. Even worse, when the rats stopped taking the carb blocker, they actually ended up eating 50% more food than before. [23]

And, herein lies the problem with so many of these “hacks” and “quick fixes” -- the assume human physiology is easily tricked, which it isn’t, by the way.

Our bodies are built to survive, and will find a way around whatever kind of carb blocker, fat blocker, or any other half-baked supplement to get what it needs to survive. This can be making more enzymes, developing a tolerance to certain compounds, or finding another way to derive energy from the foods.

And no, there’s nothing magical about “grandma’s recipe” that will make it supercede the laws of nature. As wonderful as grandma’s cooking may be, it’s not supernatural.

Side Effects of Carb and Fat Blockers

So, aside from carb and fat blockers being somewhat effect for reducing sugar and fat uptake, do they come with any drawbacks?

Given a cursory glance, most abstracts will say that carb and fat blockers are well-tolerated and come with no adverse side effects. What this means, is that the compounds tested didn’t cause the subjects to have to be rushed to the hospital because they were vomiting and bleeding from their eyeballs.

It does not mean they were without any side effects though.

Case in point, many carb blockers prevent complex carbohydrates breaking down into glucose. As a result, these carbs are sent to the colon, where they are fermented by the gut bacteria and cause all kinds of gastrointestinal effects such as bloating, flatulence and diarrhea. [24,25]

With respect to fat blockers, anyone who’s ever eaten to many potato chips with Olestra can testify as to the unsavory effects that result when you mess with the body’s fat digestion and absorption.

To put it bluntly, when you inhibit fat digestion, unabsorbed fatty acids act like intestinal lubricant, meaning you better be within three steps of a bathroom or you’re going to have one hell of a mess to clean up.

Note: This is why people taking Orlistat (a lipase inhibitor) report having “accidents” with higher than normal frequency.

The reason this happens is that the chyme (food that becomes feces) in your intestines usually takes a while to pass through, so that nutrients can be absorbed. Fats also help slow down the digestion process.

However, when fat digestion is impaired (via lipase inhibition), the track is “greased” and the next time your intestines contract to keep things moving, the chyme goes flying out the shoot, quite literally.

As if that was not bad enough, there’s another problem with some of these carb and fat blockers -- they can block micronutrient (vitamins and minerals) uptake as well.

You see, several micronutrients (Vitamins A, D, E, & K, for instance) are fat-soluble, meaning they need fat to be present to be properly absorbed. If you’re taking carb and fat blockers everytime you eat, it stands to reason that you’re inhibiting the absorption of the essential vitamins and minerals, which can lead to nutrient deficiencies down the road.

Commentary

Pharmaceutical carb and fat blockers, such as Orlistat, only block a maximum of 25% of the calories from being absorbed. So, to think that an all natural ingredient, that doesn’t require a prescription, can be included in a peanut butter and block ALL of the fat and carbohydrate calories is pure poppycock. Plain and simple.

The simple truth is that carb and fat blockers on the market aren’t very effective, and even if they were, to think that they could prevent ALL carbohydrates and fats from being digested is ludicrous. If this were true, hospitals and health insurance companies would be lining up left and right to get people to buy them and end the obesity and type 2 diabetes epidemic.

If such a compound did exist, it would be advertised around the world, and more likely, it would only be available via prescription so some company could make a huge chunk of change off of it.

Simply put, the idea of a 100% all natural carb and fat blocker supplement or food that prevents any and all carbohydrates and fatty acids from being absorbed is absurd and above all misleading to the consumer.

Instead of preaching restraint and healthy eating, promoting the idea that a product is carb free, fat-free, and guilt-free only serves to worsen the overconsumption mindset and does nothing to instill healthy nutrition protocols.

Rather than fall for another gimmick, why not learn how to enjoy real peanut butter, pizza, or any other guilty pleasure within the confines of a healthy diet. You can have your cake and eat it too, you just need to know when to put the damn fork down.

References

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2) Teng, H., & Chen, L. (2016). α-Glucosidase and α-amylase inhibitors from seed oil: A review of liposoluble substance to treat diabetes. Critical Reviews in Food Science and Nutrition, 57(16), 3438–3448. doi:10.1080/10408398.2015.1129309

3) Larner, J.; Lardy, H.; Myrback, K. (1960). "Other glucosidases". In Boyer, P.D. The Enzymes. 4 (2nd ed.). New York: Academic Press. pp. 369–378.

4) S, Chiba. "Molecular Mechanism in Alpha-glucosidase and Glucoamylase. - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/9301101.

5) Nathan, D. M., et al. (2009). Medical Management of Hyperglycemia in Type 2 Diabetes: A Consensus Algorithm for the Initiation and Adjustment of Therapy A consensus statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care. 32: 193-203.

6) Barrett ML, Udani JK. A proprietary alpha-amylase inhibitor from white bean (Phaseolus vulgaris): a review of clinical studies on weight loss and glycemic control. Nutr J. 2011;10:24. Published 2011 Mar 17. doi:10.1186/1475-2891-10-24

7) Venable, Samantha J.; Aschenbrenner, Diane S. Drug Therapy In Nursing. Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 0-7817-4839-9.

8) Yamada J, Yamamoto T, Yamaguchi T. Effects of combination of functional food materials on body weight, body fat percentage, serum triglyceride and blood glucose. 2007. http://www.phase2info.com/pdf/Phase2_Study15.pdf

9) Gupta M , et al. "Purification of a Novel α-amylase Inhibitor from Local Himalayan Bean (Phaseolus Vulgaris) Seeds with Activity Towards Bruchid Pests and Human Sali... - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/24966421.

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13) Tanabe G , et al. "In Silico Design, Synthesis and Evaluation of 3'-O-benzylated Analogs of Salacinol, a Potent α-glucosidase Inhibitor Isolated from an Ayurvedic Tra... - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/22820468.

14) Muraoka O , et al. "Quantitative Analysis of Neosalacinol and Neokotalanol, Another Two Potent α-glucosidase Inhibitors from Salacia Species, by LC-MS with Ion Pair Ch... - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/20981499.

15) ---. "In Silico Design, Synthesis and Evaluation of 3'-O-benzylated Analogs of Salacinol, a Potent α-glucosidase Inhibitor Isolated from an Ayurvedic Tra... - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/22820468.

16) Oe H and Ozaki S. "Hypoglycemic Effect of 13-membered Ring Thiocyclitol, a Novel Alpha-glucosidase Inhibitor from Kothala-himbutu (Salacia Reticulata). - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/18603797.

17) Williams JA , et al. "Extract of Salacia Oblonga Lowers Acute Glycemia in Patients with Type 2 Diabetes. - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/17616771.

18) Heacock PM , et al. "Effects of a Medical Food Containing an Herbal Alpha-glucosidase Inhibitor on Postprandial Glycemia and Insulinemia in Healthy Adults. - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/15635348.

19) Collene AL , et al. "Effects of a Nutritional Supplement Containing Salacia Oblonga Extract and Insulinogenic Amino Acids on Postprandial Glycemia, Insulinemia, and Bre... - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/15975493.

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21) Brugge WR and Rosenfeld MS. "Impairment of Starch Absorption by a Potent Amylase Inhibitor. - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/2440298.

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23) Carai MA , et al. "Potential Efficacy of Preparations Derived from Phaseolus Vulgaris in the Control of Appetite, Energy Intake, and Carbohydrate Metabolism. - PubMed - NCBI." National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/pubmed/21437128.

24) Boivin M, Zinsmeister AR, Go VL, DiMagno EP. Effect of a purified amylase inhibitor on carbohydrate metabolism after a mixed meal in healthy humans. Mayo Clin Proc 1987;62:249-55.

25) Boivin M, Flourie B, Rizza RA, et al. Gastrointestinal and metabolic effects of amylase inhibition in diabetics. Gastroenterology 1988;94:387-94

26) Jarosz, P. A., Fletcher, E., Elserafy, E., Artiss, J. D., & Jen, K.-L. C. (2013). The Effect of α-Cyclodextrin on postprandial lipid and glycemic responses to a fat-containing meal. Metabolism, 62(10), 1443–1447. doi:10.1016/j.metabol.2013.05.015

27) Buckley, J. D., Thorp, A. A., Murphy, K. J., & Howe, P. R. C. (2006). Dose-dependent inhibition of the post-prandial glycaemic response to a standard carbohydrate meal following incorporation of alpha-cyclodextrin. Annals of Nutrition and Metabolism, 50(2), 108–114. https://doi.org/10.1159/000090498

28) Wagner EM, Jen KL, Artiss JD, Remaley AT. Dietary alpha-cyclodextrin lowers low-density lipoprotein cholesterol and alters plasma fatty acid profile in low-density lipoprotein receptor knockout mice on a high-fat diet. Metabolism. 2008;57(8):1046-51.

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