Are There Good and Bad Carbohydrates Peer Reviewed

Snap Shot

When discussing carbohydrate restriction, two fallacious arguments related to the energy needs of the brain and the sustainability of a ketogenic diet are oftentimes levied against the use of a well-formulated ketogenic diet in practical therapeutic medicine:

  1. The human brain burns 600 kcal per day, and this translates to a 150 gram per day glucose requirement to encounter its free energy needs, and
  2. No one can follow a ketogenic diet long term.

In the peer-reviewed medical literature over the concluding 5 decades, these arguments confronting the safety and sustainability of nutritional ketosis have been proven false over and over again, most recently with the ii-yr results of our Indiana University Health study¹.

We have addressed the necessary components of a well-formulated ketogenic diet that most people tin follow for years if properly informed and supported. The specific topic that we want to accost here is how both the encephalon and body can function as well—or even better—on a nutrition with little or no dietary sugar compared to the typically promoted depression fat, high carbohydrate 'healthy nutrition.'

Published science has shown that ketones that are produced from either dietary fats or triglycerides stored in our adipose tissue reserves are an first-class fuel for the brain.  Further, we now know that these ketones produced by the liver also take multiple beneficial furnishings on the heart, kidneys, and other organs that appear to translate into improved longevity²,³,⁴. Additionally, new research has highlighted that skeletal muscles, even those of competitive athletes, are not solely dependent on high dietary carbohydrate intake for glycogen replenishment and functioning⁵.

However, up until 5 years ago, nevertheless, we struggled to understand the mechanism(s) of these additional beneficial effects. At present we know why this long-discounted physiology can play a dominant role in our health and well-being.  In addition to the fact that ketones are a cleaner-burning fuel (i.e., producing fewer complimentary-radicals) than glucose when used by the brain and other organs, the primary ketone beta-hydroxybutyrate can besides function every bit a point to actuate genes that regulate our defenses against oxidative stress and inflammation³.

How the trunk shifts its primary energy source from carbohydrates to fats and ketones is anything but simple. This process, which we have named 'keto-accommodation,' starts inside days simply takes a considerable menstruation of time to fully develop. And even afterwards information technology is complete, the result is not an absolute exclusion of glucose from the body's fuel supply. Rather, the demand and use of glucose is dramatically reduced, while at the aforementioned fourth dimension pathways that save products of partially metabolized glucose (e.thousand., pyruvate and lactate) for recycling into fuel and other beneficial metabolic intermediates become more finely tuned. The result is maintenance of normal blood glucose and musculus glycogen levels that tin be sustained without the need for dietary carbohydrate intake.

Physiologic Role of Carbohydrates

The conventionalities that the encephalon and central nervous system need carbohydrates to function properly is oft supported with the circular logic that the brain uses glucose therefore it needs glucose, and it needs it considering it uses it. The hole in this statement is that the brain does non in fact need glucose. Information technology actually functions quite well on ketones. Stating it some other way, the presumed requirement for glucose by the brain is a provisional need that is based on the fuel sources dictated by one's selection of nutrition. A ketone-suppressing diet (i.east., any diet supplying >30% of energy from the combined intakes of carbohydrate and protein) essentially forces the brain to rely on glucose for fuel.

It is true that some cells inside the body do crave glucose. For example, red claret cells, parts of the kidney, and the epithelial cells that comprehend the lens of the eye are primarily glycolytic because they lack mitochondria and thus are dependent upon glucose to office. This is too partially true for the fast-twitch muscle fibers (which have fewer mitochondria than wearisome-twitch muscle) used for loftier intensity practice like weight lifting and sprinting. Only in all of these cases where glucose is broken downward to lactate, the body and so has a pick—cells with mitochondria tin further oxidize the lactate to CO2 and water, or the trunk tin recycle that lactate back to glucose.

Show That the Brain Tin can Function on Ketones

The simplest experiment that demonstrates the brain'south ability to role on ketones is the observation that humans can tolerate total fasting with normal mental function for durations of 30-sixty days. Interestingly, during prolonged starvation, muscle mass and other of import structures in the trunk progressively lose mass and function. The brain, nonetheless, is fully protected against the starvation catabolism that depletes the rest of the body.  Elegantly done studies that measured glucose and ketone levels in arterial blood going into the brain compared to these fuels in the jugular vein coming out of the brain, indicated that ketones are in fact able to supply the great bulk of the brain'due south energy. But because even prolonged starvation does not reduce the blood glucose level below the 'depression normal' range, these observations did not prove there is not a small but significant glucose requirement for the keto-adjusted brain.

This question was addressed directly many decades ago when ii prominent enquiry groups undertook similar experiments to evaluate mental function in starvation-adapted patients whose blood glucose was reduced to very depression levels by an infusion of insulin⁶,⁷.

[Although we are sharing this as valuable published information, nosotros besides need to note that while these experiments were considered adequate in the twenty-four hours, they would not laissez passer ethical muster today due to the risks for the patients compared to the benefits of the accrued knowledge.]

Both studies involved severely obese patients who had been on full fasts under continuous inpatient observation for from 30 to lx days. In the written report by Drenick et al., 9 participants with blood BOHB (beta hydroxybutyrate) in the 7–viii mM range were administered a single bolus of insulin sufficient to transiently drive blood glucose values downwards to a mean of 36 mg/dl (with some patients' values going as low as 9 mg/dl). Despite causing profound hypoglycemia to levels normally associated with coma or death, none of these patients experienced any symptoms associated with hypoglycemia. Moreover, measures of urinary catecholamines that are indicative of the torso's counter-regulatory stress response to hypoglycemia were not elevated, despite these brief but greatly low blood glucose values.

In the other study reported by Cahill and Aoki⁷, 3 obese males adapted to prolonged fasting were administered insulin via a slow constant infusion over 24 hours. In this case, blood glucose levels declined gradually, but eventually reached a mean value of 25 mg/dl, while blood BOHB stayed in the 4–6 mM range. With this method of insulin administration, claret glucose values under 36 mg/dl were sustained for 10–12 hours, but once again the patients exhibited no clinical signs of hypoglycemia or a counter-regulatory hormonal response.

What these two dramatic (but risky) studies demonstrated is clear evidence of normal brain office in the virtual absence of glucose when sufficient ketones are available. This offers us the unique perspective that when consuming a sugar-rich diet, the predominate source of fuel for the brain is glucose; not because information technology is needed only because the other natural and highly effective encephalon free energy source has been shut off. Simply nether weather of consequent nutritional ketosis, the brain adapts to the presence of ketones by enhancing their uptake and oxidation, thus protecting cognitive and CNS part⁶.

It should be noted that these studies showing potent neuro-protection by ketones under conditions of profound hypoglycemia involved small groups of patients with claret ketones in the 4–viii mM range, whereas nutritional ketosis values tend to exist lower—i.eastward., in the 1–4 mM range. We do not take the results of similar man studies with purposefully-induced hypoglycemia, and modernistic ethical standards accordingly prevent such inquiry.  However, in managing numerous patients with type two diabetes taking hypoglycemic medication, nosotros have observed many instances of moderate hypoglycemia without the expected symptoms when blood BOHB values are in the nutritional ketosis range. Besides of note, is the fact that the brain favors ketones over glucose as indicated by preferential uptake of ketones fifty-fifty when glucose is elevated⁸. This too appears to be the instance in the heart.

Essentials of Keto-Adaptation—Glucose Conservation and Salvage

Information technology is important to remember that simply because one doesn't eat dietary carbohydrate does non mean the trunk is completely defective in glucose. Whether on a total fast for weeks⁶,⁷ or following a meat-and-fat-merely ketogenic diet for a month⁹,¹⁰, blood glucose values remain in the normal range both at remainder and during do. This occurs considering the body is quite capable of synthesizing all of the glucose it needs from various gluconeogenic precursors, while at the aforementioned fourth dimension strictly limiting its rate of carbohydrate oxidation.There are at least v sources of these glucose precursors:

  1. breakup of muscle to supply amino acids for gluconeogenesis;
  2. breakdown of dietary protein to supply amino acids for gluconeogenesis,
  3. glycerol released from the hydrolysis of adipose tissue triglyceride or dietary triglyceride;
  4. recycling lactate and pyruvate from glycolysis; and
  5. acetone produced past the spontaneous breakdown of acetoacetate to acetone that can be used for gluconeogenesis.

This last source is a bit surprising, as it is actually a small simply significant pathway for the production of glucose from fatty acids¹¹. The conditions for and the amounts provided past these diverse sources of gluconeogenesis are shown in the following table.

What this table clearly demonstrates is that whether during a total fast or a ketogenic diet without sugar containing foods, new or recycled gluconeogenic substrates provide for the generation of anywhere from 100–200 g/d of glucose. Add to this upwardly to 50 grand/d of dietary carbohydrate as part of a well-formulated ketogenic diet, and it becomes clear why nutritional ketosis is well tolerated under a diverseness of challenging conditions.

The obligate other one-half of this balancing equation is the torso's ability to strictly limit its internet use of glucose as an oxidative fuel. The extent of this conservation tin can exist appreciated from indirect calorimetry data from keto-adapted adults at residue and during endurance exercise. In both untrained and highly trained individuals, this indicator of full trunk fuel employ shows that approximately 90% of the body's energy is being supplied past fat or ketones derived from fatty⁵,⁹,¹⁰.

Lessons from Low Carbohydrate Athletes

Perhaps the situation perceived every bit well-nigh challenging for someone on a ketogenic diet is the power to maintain glucose/glycogen reserves with prolonged, high intensity practice. For a greater part of the last century, the accepted paradigm has been that i's initial muscle glycogen is positively correlated with the ability to sustain endurance functioning during moderate-to-high intensity exercise¹²,¹³. Even so, given that fifty-fifty with 'optimized' muscle glycogen obtained by using a carbohydrate-loading diet strategy, an endurance athlete has a pinnacle total trunk glycogen content of only about 2000 kcal. To attempt to simultaneously train the muscles to use more fat and reduce one'southward dependency upon glycogen in order to extend performance creates somewhat of a metabolic oxymoron. This is because very high insulin levels induced past sugar loading actually suppress adipose fatty acid release and oxidation.

To explore this further and assess the limits of man fat oxidation during exercise, a research team from the Netherlands studied 300 adults, examining their maximum fat oxidation during exercise¹⁴. They reported the maximum rate of fat oxidation for the best private fatty burner in this group (which included a number of highly trained athletes) to be 0.99 grams of fatty per minute. However long before that, one of the states reported that bike racers who were keto-adapted for but 4 weeks were able to fire fat at one.v grams of fat per minute¹⁰. Based upon the before and subsequently musculus biopsies taken in this report, after keto-adaptation these bike racers were able to perform the aforementioned corporeality of work while using just one quarter the amount of muscle glycogen. This was the start study that conspicuously disconnected musculus glycogen from endurance performance in keto-adapted athletes.

All the same, the all-time sit-in of this disconnect was recently published by Jeff Volek'south grouping⁵. Nosotros recruited twenty competitive ultra-runners, 10 of whom followed a traditional loftier saccharide nutrition and the other 10 had been following a ketogenic diet for at least 6 months (mean diet duration 22 months). The ketogenic diet group reported an average daily carbohydrate intake of 64 grams and had a mean fasting serum BOHB of 0.6 mM.

After baseline testing, these runners were asked to do a 3-hr run at race-pace on a treadmill—essentially an indoor marathon. Surprisingly, both groups had similar musculus glycogen levels earlier the run, and they besides both mobilized similar amounts (about 80%) of their glycogen during three hours on the treadmill. But indirect calorimetry testing (measuring 02 consumption and CO2 production) indicated that almost 90% of ketogenic runner's internet energy use was from fat. This effect is a clear indication that glycogen mobilization does not equate with carbohydrate oxidation in the keto-adapted state. Rather glycogen stores can be optimized and available for anaerobic (aka glycolytic) musculus part and so quantitatively recycled dorsum to glucose by the liver. An even more than amazing example of beingness able to maintain normal muscle glycogen while consuming very little sugar during repeated days of exhaustive exercise has been reported in trained sled dogs¹⁵,¹⁶.

Why Some Experts Still Claim that We Need Dietary Carbohydrates

In addition to the commonly stated but flawed arguments for dietary carbohydrate that we have addressed above—i.east., that the brain and some other tissues are obligate carbohydrate burners and that carbohydrates are required for exercise—there are a number of other reasons often used to support the idea that nosotros need to swallow carbohydrates above levels that facilitate nutritional ketosis.

The liquid poly peptide diet debacle. With the publication of the book 'The Last Chance Diet' in 1976, a profoundly flawed nutrition with overt electrolyte and mineral inadequacies was promoted to the public, resulting in over lx cases of sudden death reported to the CDC in the following few years. Rather than actually identifying the true underlying cause, skillful opinion was that ketones were toxic to the center¹⁷,¹⁸. Despite our publishing multiple rigorous studies demonstrating excellent maintenance of heart rhythm and function when adequate electrolytes and minerals are supplied during nutritional ketosis⁵,⁹,¹⁰,¹⁹ this flawed conclusion remains normally held past many medical practitioners and scientists to this day. That withal, there is absolutely no scientific basis for the claim that dietary carbohydrates are necessary to prevent the buildup of damaging levels of ketones (AKA 'toxic byproducts of fatty metabolism').

The myth of adrenal fatigue. In both general clinical experience and in some published research, poorly formulated low carbohydrate diets are understood to crusade headache, fatigue, do intolerance (aka 'keto flu), and adrenergic depletion (20). This study by DeHaven—The Yale Turkey Report—has been discussed in our prior weblog post. In brief, they administered a protein-only nutrition to obese women for iv–6 weeks containing severely restricted amounts of sodium and potassium. The resulting impaired protein metabolism and profound hypotension was due to overt electrolyte inadequacies, non nutritional ketosis as the authors merits. These and other findings presented where subjects did not receive adequate electrolyte replacements have been used to paint a movie of physiological stress that can be brought on by a ketogenic nutrition, despite numerous studies indicating no increased catecholamine response in keto-adapted subjects⁶,⁷.

Thyroid dysfunction secondary to nutritional ketosis. In the context of the common observation of dumb energy and exercise tolerance when nutritional ketosis is combined with inadequate intakes of electrolytes, it is tempting to blame this on dumb thyroid function. However, this common determination does non stand upward to basic scientific scrutiny. Yes, the blood level of the active thyroid hormone T3 typically falls by 30–40% in the showtime few weeks of a well-formulated ketogenic diet, but this is non accompanied past any signs or symptoms of clinical hypothyroidism. As discussed in our prior weblog post Does Your Thyroid Need Dietary Carbohydrates?, this alter is due to a marked reduction in thyroid hormone resistance (similar to the concurrent improved insulin resistance) during nutritional ketosis. Therefore, this is a healthy response and non a sign of endocrine dysfunction.

Slumber patterns are disturbed past a ketogenic nutrition. Many people report that they sleep less when in nutritional ketosis. We take recently addressed this question in a report of our patients in the Indiana University Health study. Nosotros found that global sleep quality, sleep disturbances, and daytime dysfunction parameters all were significantly improved. In addition, the proportion of patients reporting poor sleep was significantly reduced after 1 year²¹. A partial explanation for the mechanism of these benefits may exist that the brain'due south animate response to CO2 buildup is improved during nutritional ketosis²².

Nosotros need more dietary fiber than is possible on a ketogenic diet. In add-on to promoting colon health, there is at present stiff evidence that short-chain fatty acids (SCFAs) produced from colonic fermentation of fiber likewise improves brain wellness. And it is indeed true that the combination of a very high cobweb intake plus adequate carbohydrate restriction to sustain nutritional ketosis is difficult to attain without the apply of purified cobweb supplements. But what we point out in our blog postal service on cobweb is that the production of beta-hydroxybutyrate can provide many-fold more SCFAs to the brain than a very high fiber diet combined with an optimized microbiome. Thus, the moderate level of fiber that one can achieve with a real-food well-formulated ketogenic diet should be more than adequate to maintain organ wellness throughout the torso.

Conclusions

The need for dietary carbohydrates is often a topic of misunderstanding and misinformation. Although some specific tissues in the body do have certain glucose requirements, these requirements are easily met by gluconeogenic sources inside the trunk without the need for dietary carbohydrate intake. There are also some people who claim a behavioral 'need' for breadstuff, just that soon passes after a few weeks of keto-adaptation. The fatigue, stress, dumb knowledge and reduced performance that are often used to argue for the need for carbohydrate are more aptly owing to improper implementation of a well-formulated ketogenic diet, inadequate electrolyte replacement, and/or insufficient time for keto-accommodation. When used correctly, a ketogenic diet can be a condom and sustainable therapeutic tool also every bit a means to help promote wellness and performance.

The information we provide at virtahealth.com and weblog.virtahealth.com is not medical communication, nor is it intended to replace a consultation with a medical professional person. Delight inform your physician of whatever changes you brand to your diet or lifestyle and discuss these changes with them. If you lot accept questions or concerns virtually any medical weather y'all may have, please contact your physician.

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Source: https://www.virtahealth.com/blog/why-dont-need-dietary-carbohydrates

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