High-Fat, Low-Net-Carb Bar

High Fat, Low Net Carb Snack Bar

Most energy bars’ caloric composition includes high levels of net (i.e., non-fibrous) carbohydrates, moderate levels of protein, and low levels of fat. At IQ Bar, we flip this convention on its head. Our bars’ dominant macronutrient is fat, and we keep net carbs low (8-9g/bar) by excluding grains and added sugars. One carb that is highly present in IQ Bars is fiber (see why in our Critical Nutrients section), which we keep at a ~2:1 ratio with natural sugar. Read up on why we chose a high-fat, low-net-carb profile below.


Important Note: When we talk about “fat” we are NOT referring to trans fat, a variety that's been almost universally deemed to negatively impact health. IQ Bars contain zero trans fat.

Brain Health

Not only is the brain the fattiest organ in the body (at 70% fat), but vitamins critical to brain health - like A, D, E and K - cannot be absorbed without dietary fat. Thus, it’s no surprise that a high-fat diet correlates with cognitive health benefits. In our IQ Bar Nutrients section, we detail benefits of specific fats like omega-3’s. In addition, though, numerous studies have uncovered positive long-term effects of high-fat diets in general. For instance, a seminal 1998 post-mortem study found that control patients had vastly greater fat content in their cerebrospinal fluid relative to Alzheimer’s patients. [1] A more recent, 2012 study found that older people whose diets were highest in fats were 42% less likely to develop mild cognitive impairment (MCI), a condition widely considered to be a precursor of Alzheimer’s. [2]

Perhaps the greatest testament to fat’s beneficial cognitive impact is that it is regularly used to treat serious neurological conditions. For instance, a high-fat, “ketogenic” diet has been used to treat epileptic seizures for thousands of years, and has, according to recent studies, led to an up-to-90% reduction in seizure frequency for many patients. [3][4][5] Another 2005 study found that Parkinson’s disease patients experienced a 43% reduction in Unified Parkinson’s Disease Rating Scale scores after being on a high-fat diet. [6] A 2014 study even found that a ketogenic diet counteracted migraines, reducing their frequency by 76% and their length of attack by 82%. [7] Thus, when presented with biological assailants, it appears the brain craves the same compound it is comprised of: fat.

Chronic carbohydrate intake, on the other hand, has been linked with adverse cognitive outcomes. In the aforementioned 2012 study on MCI, subjects in the highest-carb group were nearly four times more likely to be impaired than those in the high-fat group [2]. A second 2012 study found that healthy, non-diabetic subjects with the highest blood glucose levels - a hallmark of high carb consumption - had smaller hippocampi and amygdalae, brain structures critical to memory and emotion. [8] To help us understand many of the reasons why carb-induced blood sugar spikes can injure the brain, neurologist David Perlmutter gets specific in his 2013 best-selling book Grain Brain:

When your blood sugar increases, there’s an immediate depletion of the neurotransmitters serotonin, epinephrine, norepinephrine, GABA, and dopamine. At the same time, B-complex vitamins, which are needed to make those neurotransmitters (and a few hundred other things), get used up. Magnesium levels also diminish, and this handicaps both your nervous system and liver. In addition, high blood sugar triggers a reaction called ‘glycation,’...the biological process whereby glucose, proteins, and certain fats become tangled together, causing tissues and cells to become stiff and inflexible, including those in the brain. [9]

Sustained Energy

Fat has served as a primary bodily and cognitive energy source for over 99% of humans’ two-and-a-half million year evolution. Our hunter-gatherer ancestors thrived on a diet consisting of roughly 75% fat, and it wasn’t until 10,000 years ago - a blip in our species’ history - that modern agriculture introduced fat-displacing foods like grains to the human diet. Moreover, it wasn’t until the 1970’s, when the US Senate Committee on Nutrition and Human Needs began pushing carbohydrates (largely through their “Dietary Goals for the United States”), that the low-fat diet gained serious traction in America. Thus, from an evolutionary standpoint, it’s fair to say we are still “pre-programmed” to run on fat, and there’s quite a bit of research to support that position.

For one, fat is essential to survival. Were we to go entirely fat-free, we would perish. By contrast, carbs are non-essential, as our bodies can generate their derivative glucose from protein via gluconeogenesis. In addition, fat offers a highly concentrated form of energy, with more than double the potential energy per gram that carbs and protein offer. That energy, when delivered through fat-derived ketone bodies, is also highly efficient. As Harvard Medical School professor George Cahill notes: “Studies have shown that beta-hydroxybutyrate, the principal ketone, is not just a fuel, but a superfuel, more efficiently producing ATP energy than glucose.” [10] As an example, Cahill cites an animal study showing ketones to provide  unmatched contractility (strength and vigor) in the heart per unit of oxygen consumed. [11]

Fat is also the longest-lasting, most even-burning form of macronutrient energy. When the body burns fat, it draws on a virtually endless source of fuel. Because fat doesn’t need to be stored with water - as carbohydrates do - even the leanest of bodies can retain up to 100,000 calories of it (by contrast, we can store just a few thousand calories of carb-derived glycogen). Thus, it makes sense that a body at rest or engaged in moderately-intense exercise draws the majority of its energy from free fatty acids and muscle triglycerides. [12] Moreover, because fat consumption does not meaningfully elevate blood glucose, a higher-fat diet can spare our bodies from volatility in energy levels. Unlike carbohydrate metabolism, fat metabolism is a slow-release process with an effectively bottomless reserve fuel tank.

The Preferred Fuel?

Some in the health, nutrition, and fitness spaces have deemed carbohydrates to be the human body and brain’s “preferred” source of fuel. Here, we’ll address two arguments commonly made by those who assert this position, and provide IQ Bar’s responses to these arguments:

Pro-Carb Argument #1: Our body metabolizes carbohydrates before fats. Thus, carbohydrates must be our body’s preferred fuel source.

IQ Bar’s Take: If this logic was valid, our bodies’ truly preferred energy source would be alcohol. After all, when we consume alcohol with food, our body metabolizes the alcohol before any other energy source - carbohydrates included. Of course, we all know alcohol is not a desirable energy source, and has numerous deleterious health impacts when consumed at volume. Moreover, a primary reason our body burns carbs before fat is our need to keep blood glucose levels from becoming poisonously high after a meal. The point here is that we at IQ Bar feel the moniker of “preferred energy source” should not be defined by speed of metabolism, but rather by factors such as how dense, clean-burning, and efficiently stored the energy source is. And, in all of these categories, fat is the clear frontrunner.

Argument #2: The brain runs almost exclusively on glucose, and cannot use fatty acids as fuel. Thus, carbohydrates must be our brain’s preferred fuel source.

IQ Bar’s Take: Our brain does, in fact, run almost exclusively on glucose when we consume a high-carb diet, and it is true that fatty acids cannot be burned as brain fuel, as they cannot pass the blood-brain barrier. However, when glucose and its stored form glycogen are low, the liver readily converts fatty acids into ketone bodies, which can displace glucose as a primary (and arguably more efficient) source of brain fuel. Furthermore, when medium-chain triglycerides (MCT’s) are consumed, they are converted by the liver into meaningful quantities of brain-fueling ketones regardless of carbohydrate and glycogen levels. [13] Some brain cells do require glucose-based energy, though this does not have to come from carbs - it can be generated by breaking down proteins and other compounds via gluconeogenesis.

Eat Fat, Be...Thin!

Unfortunately, when most people think of the word “fat”, images of obesity are conjured. Yet consuming a high-fat diet has actually been shown to correlate with weight-loss, not gain. Numerous studies have shown that a high-fat diet results in far greater weight loss than a low-fat diet [14][15][16][17][18]. The true driver of fat accumulation and retention appears to be the carbohydrate. Of course this is by no means a novel realization. Hugely popular modern weight-loss regimens like the Atkins, Paleo, Whole-30, and ketogenic diets are all predicated on the same principle: cut the carbs. So what is it about carbohydrates that cause us to get fat?

After ingestion, carbs are converted into glucose and enter the bloodstream. Only some of this glucose can be burned for energy - our pancreas secretes insulin into the blood to ferry the excess into liver, fat, and muscle cells that convert some of it into glycogen, and much of it into fat. Insulin also promotes the formation of new fat cells, and the retention of fat via several mechanisms. First, it facilitates triglyceride formation in fat cells by increasing volumes of cellular glycerol. Second, it stimulates fatty-acid-attracting enzyme lipoprotein lipase (LPL) in fat cells, causing them to grow, and tempers LPL in muscle cells, reducing their ability to burn fatty acids. Third, it suppresses hormone-sensitive lipase (HSL), an enzyme that breaks down fat cell triglycerides into fatty acids that can enter the blood and be used for fuel.

Fat ingestion, by contrast, does not trigger meaningful insulin release, and thus does not promote fat retention. When we consume a high-fat meal, triglycerides enter the blood (via chylomicron particles) where they are either broken down into fatty acids and used for energy by muscle cells, broken down and stored in muscle and fat cells, or transformed into other substances in the liver and recycled back into the blood. However, because this meal does not upregulate insulin and re-balance LPL and HSL to support fat retention, the fat we temporarily store after eating can easily flow back into the blood to be burned for energy between meals. Moreover, a high-fat diet has been shown to temper the hunger hormone ghrelin, and correlate with lower reported hunger levels, keeping our appetite in check. [19][20]

 

REFERENCES:

  1. Mulder M, Ravid R, Swaab DF, et al. Reduced levels of cholesterol, phospholipids, and fatty acids in cerebrospinal fluid of Alzheimer disease patients are not related to apolipoprotein E4. Alzheimer's Disease and Associated Disorders. 1998;12(3):198-203 (Link)
  2. Roberts RO, Roberts LA, Geda YE, et al. Relative Intake of Macronutrients Impacts Risk of Mild Cognitive Impairment or dementia. Journal of Alzheimer’s disease : JAD. 2012;32(2):329-339. doi:10.3233/JAD-2012-120862. (Link)
  3. Hemingway C, Freeman JM, Pillas DJ, et al. The Ketogenic Diet: A 3- to 6-Year Follow-Up of 150 Children Enrolled Prospectively. 
  4. Freeman JM, Vining EP, Pillas DJ, et al. The efficacy of the ketogenic diet-1998: a prospective evaluation of intervention in 150 children. Pediatrics. 1998;102(6):1358-63 (Link)
  5. Marsh EB, Freeman JM, Kossoff EH, et al. The outcome of children with intractable seizures: a 3- to 6-year follow-up of 67 children who remained on the ketogenic diet less than one year. Epilepsia. 2006;47(2):425-30 doi:10.1111/j.1528-1167.2006.00439.x (Link)
  6. Vanitallie TB, Nonas C, Di Rocco A, et al. Treatment of Parkinson disease with diet-induced hyperketonemia: a feasibility study. Neurology. 2005;64(4):728-30 (Link)
  7. Lorenzo CD, Coppola G, Sirianni G, et al. Migraine improvement during short lasting ketogenesis: A proof-of-concept study. European Journal of Neurology. 2014;22(1):170-177 doi:10.1111/ene.12550 (Link)
  8. Cherbuin N, Sachdev P, Anstey KJ, et al. Higher normal fasting plasma glucose is associated with hippocampal atrophy: The PATH Study. Neurology. 2012;79(10):1019-26 doi:10.1212/WNL.0b013e31826846de. (Link)
  9. David Perlmutter, MD, Grain Brain (New York, Boston, London: Little, Brown and Company, 2013). p.82-83
  10. Cahill GF, Veech RL. Ketoacids? Good medicine? Transactions of the American Clinical and Climatological Association. 2003;114:149-163. (Link)
  11. Kashiwaya Y, Sato K, Tsuchiya N, et al. Control of glucose utilization in working perfused rat heart. Journal of Biological Chemistry. 1994;269(41):25502-14 (Link)
  12. Romijn JA, Coyle EF, Sidossis LS, et al. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. American Journal of Physiology. 1993;265(1):380-91 (Link)
  13. Courchesne-Loyer A, Fortier M, Tremblay-Mercier J, et al. Stimulation of mild, sustained ketonemia by medium-chain triacylglycerols in healthy humans: estimated potential contribution to brain energy metabolism. Nutrition. 2013;29(4):635-40 (Link)
  14. Volek J, Sharman M, Gómez A, et al. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutrition & Metabolism. 2004;1:13. doi:10.1186/1743-7075-1-13. (Link)
  15. Samaha FF, Iqbal N, Seshadri P, et al. A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity. New England Journal of Medicine. 2003;348:2074-81 doi:1056/NEJMoa022637. (Link)
  16. Sondike SB, Copperman N, Jacobson MS. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. The Journal of Pediatrics. 2003;142(3):253-258 doi:http://dx.doi.org/10.1067/mpd.2003.4. (Link)
  17. Brehm BJ, Seeley RJ, Daniels SR. A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. Journal of Clinical Endocrinology & Metabolism. 2003;88(4):1617-23 doi:10.1210/jc.2002-021480 (Link)
  18. Volek JS, Phinney SD, Forsythe CE. Carbohydrate Restriction has a More Favorable Impact on the Metabolic Syndrome than a Low Fat Diet. Lipids. 2009;44:297 doi:10.1007/s11745-008-3274-2. (Link)
  19. Sumithran P, Prendergast LA, Delbridge E. Ketosis and appetite-mediating nutrients and hormones after weight loss. European Journal of Clinical Nutrition. 2013;67:759-764 doi:10.1038/ejcn.2013.90 (Link)
  20. Gibson AA, Seimon RV, Lee CM, et al. Do Ketogenic Diets Really Suppress Appetite? A Systematic Review and Meta-Analysis. Obesity Reviews. 2014;16(1):64-76 doi:10.1111/obr.12230 (Link)
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