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Keto for Athletes: Yes or No?

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Keto for athletes

In our first post, Keto Dieting: Understanding the Basics, we discussed variations of keto dieting and looked at how keto diets affect clinical and non-clinical populations. Overwhelmingly, data suggest that there are health benefits for both populations. However, perhaps the most convincing argument against carbohydrate restriction and keto diets concerns athletic performance due to the athlete’s reliance on carbohydrate for fuel. In this post, we will investigate the role of keto dieting in athletic performance. As a matter of course, instead of searching for the “why or why not use keto as an athlete,” I prefer to take what is an obviously (to me) healthier diet and explore questions such as, “how many carbs can I eat on a keto diet … as an active person or athlete? or “can I optimize my performance while sustaining ketosis?”

The Use and Purpose of Dietary Fuels

Ketogenic diets are severely devoid of carbohydrate. Well, at least that is what we tend to think. From the diet’s inception, it has been restricted to 20-50g total carbohydrate per day. Only recently have a few individuals begun to question if that limit is necessary and under which conditions ketogenesis, and a greater carbohydrate, intake may occur simultaneously.

Why would we do such a thing?! If carbohydrates are bad, then they are just bad, right? And if they are bad, then shouldn’t we want to avoid them all. Period. While still less egregious than making the same association about fat, such as with the last nutritional paradigm, it is not a dichotomous situation. Carbs have a role. Fat has a role. I would argue that fat has a much more important role, but we cannot forget about carbohydrate altogether.

We have essential fats. We have essential amino acids. We have no essential carbohydrates. Still, they are widely considered the “base of human nutrition.” Since you can’t hear my tone in your head, read “base of human nutrition” with a low, sarcastic, and pompous sarcastic tone. In biological terms, “essential” means something that we need to eat because our bodies require it to survive and they cannot manufacture it on their own.

Put differently, without eating fat and protein, we die. Without eating carbohydrate, we don’t die. Are our lives rich and fulfilled? Maybe – it depends who you ask, how long they’ve lived following a carbohydrate-unrestricted eating pattern, their activity/athletic levels, and other factors. Some of you are thinking, “Hey! Fiber!” Fiber is not essential either. It’s fine; it’s just not essential. Sugar is not essential. Starch is not essential. Whole wheat is not essential. Not essential. Not essential. Not essential. Understand?

The Physiological Role of Carbs

Just because they are not essential, does not mean they are useless. Carbohydrates are an energy source. They are used to make ATP, which our cells use to do all the cool things they do. Carbs are our “preferred” energy source because they don’t do anything else, and as a result of circumstance (eating high carb diets), they are observed as being metabolized at high rates – hence “preferred.”

Carbs make ATP now, or they are stored to make ATP for later. If muscle and liver cells are full of glycogen, carbs are converted to fat to be stored, but they are not as easily converted back. Luckily, our metabolisms are flexible, or at least, they are flexible as long as we don’t screw it up!).

Still, the creation of new glucose (gluconeogenesis) is possible, and this process can satisfy all of our carbohydrate needs. It is often said that our brain cells need more than can be supplied through this process. However, that is not entirely true. Humans can fast for hundreds of days and be just fine because any unmet carbohydrate needs are satisfied by ketones. That only leaves the blood cells which require carbs, and when we fast, all our blood does not dry up, so that theory doesn’t hold any water either.

An Evolutionary Aside

If we have essential fats and essential proteins, but we have no essential carbs, which do you think we evolved consuming? Which of the three were available in great enough quantity and frequency to support life such that we did not evolve the processes necessary to create them endogenously?

Bioenergetics, Briefly

Carbohydrates serve as an energy (calorie) source. Most of those living in the United States do not require any more energy than they are already getting. Over 70% of adults are overweight, and this number continues to increase. Calories in, calories out (CICO) is not a bioenergetic law, but it is still a rule that cannot be ignored. Eating too much still yields unpleasant consequences. However, we have to consider the calories out half of the equation.

We are only going to meaningfully increase calories expended (out) via exercise or other methods of physical activity. Certain types of exercise have specific dietary needs. One of the needs can be carbohydrate. There are levels to this.

At rest, we use a mix, about 50/50 to 65/35 of fat and carbohydrate, respectively, for our ATP needs (changes with training status, but even more with diet – up to 100% fat with carbohydrate restriction). As we start exercising, the rate of energy expenditure increases, but the mix stays the same. To a point.

As exercise intensity (speed, weight) increases, metabolic needs start to switch over to anaerobic glycolysis more exclusively. This means we burn more carbs. It’s not that we use less fat, fat burning increases until it “maxes out” then the extra energetic demand is made up from carbs. On a related note, the “fat burning zone” on cardio machines is not the most effective for losing body fat. It is simply an indicator of how fast as you can go before carbohydrate utilization goes up. Consider the recent popularity of HIIT style of exercise. This involves going way over the “fat-burning zone,” yet many feel it provides greater fat loss effects.

The point is that different exercise intensities utilize different fuel sources. At rest, we use about 50% fat 50% carbohydrate, and that changes to nearly 100% fat with keto-adaptation. During exercise, carbohydrates are still required when exercise intensity exceeds the “fat-burning zone.” In practical terms, if your exercise intensity makes you “feel the burn,” you’re using carbohydrates as fuel, and a lot of them. That is a great indicator that you are working hard. However, if the carbs are not available, you have a metabolic barrier to hard work – you can only perform the action if the fuel (carbs) are there to use.

Therefore when carbohydrates are in short supply, exercise performance suffers and higher intensity exercise performance, in particular, is impaired. However, with keto-adaptation, this does NOT appear to be the case. Nonetheless, most studies examining a ketogenic diet still find it detrimental to initial power output – the amount of force a muscle can create in an instant at the beginning of exercise. This adverse effect to power output is completely recovered once carbohydrate are added to a ketogenic diet. The trick is balancing.

A New Rule of Keto for Athletes

Referencing back to part 1 of this series, “a” ketogenic diet is not “the” ketogenic diet. Athletes, individuals with large calories (as carbohydrate) out, have a need for more carbohydrate, and they can maintain ketosis while meeting that need.

One of the first reports of this was indirect. Volek compared the metabolic characteristics of elite endurance athletes consuming a ketogenic diet or a typical high carbohydrate diet. The ketogenic athletes consumed over 80g per day of carbohydrate, equivalent to 10% of their total energy intake. Now consider variance. The exact data is 82 ± 62 grams per day. Thus, while some are keeping their diet strict – “the” keto diet – others are having success eating 140g per day (~2g/kg bodyweight) or more, as that’s only one standard deviation from the mean.

Keep in mind that these are ELITE endurance athletes. This is not for everyone. However, the study highlights a very important point. “The” diet has not been adapted for all populations, and it stresses that exercise, a healthy activity that we should all be doing(!), accommodates greater carbohydrate consumption.

As previously mentioned, my dissertation research included targeted carbohydrate intake as part of participants ketogenic diet. We tested escalating doses of carbohydrate in conjunction with exercise while participants were consuming a ketogenic diet as well. All participants maintained ketosis when consuming 20g pre-exercise, and some (about 10%) maintained ketosis consuming 60g. That is 10g over “the” diet’s limit in addition to the carbs consumed from the rest of their diet. They were eating about 1g/kg bodyweight or half as much as the athletes. As a percentage of calories, the carbohydrate-based controls ate about 50% carbs, 25% fat, 25% protein. The keto diets consumed between 5-15% carbs, 63-70% fat, and 22-25% protein. Ranges are provided to show the base keto diet as well as with the addition of 60g supplemental carbs. Most aspects of performance can be maintained with the base keto diet, but others, such as peak power output, needed at least the 20g added back in. Again, these data are in review.

Population sample is important. In the first example, we have elite athletes, and in the second example, recreationally trained college kids. Although I can personally guarantee that the participants in my study were trained hard, the workload does not compare to the best ultra-endurance athletes in the country. However, the information still helps us establish the pattern. Carbohydrates are activity dependent.

What Carbs Were Allowed?

Although a keto diet can be a carnivore diet, we generally still want to encourage sufficient vegetable consumption. Quick aside: you’re only allowed to be carnivore if you eat liver and other organ meats. In my work just described, all participants had a fiber goal, and in the keto groups, the fiber goal for the men was 18g and 15g for the women. While fiber is generally healthy, in research it is simply used as a marker to indicate diet quality, not so much for its own effects. Since fiber is fermented to fat anyway, I encourage the net carb calculation (total carbs minus fiber). Participants were instructed that the major contributors to their net carb counts should be nuts, seeds, avocado, coconut, olives, and low-carb vegetables, such as broccoli, celery, peppers, onions, salad greens, etc.

For those of you who already do that and want the “extra” carbs for performance, we used a pea starch called Carb10®, which is available as a supplement (disclaimer, I now sell one [as a result, not a cause, of the research] under Archetype Nutrition). I also recommend honey, rice, fruits, and even cookies as other options as long as you are responsible about it.

A Ketogenic Diet for the Healthy

In order to support different lifestyles, “the” diet needs to be adapted. We need to go beyond the rigid limits and let the diet be based on what it produces. A ketogenic diet can have all the characteristics and results of the ketogenic diet while permitting a more flexible and athletic lifestyle.

Encompassed within this, is metabolic flexibility in general. The standard American diet programs our metabolisms to use carbohydrate while “forgetting” how to use fat for ATP generation at high rates. Long term adherence to ketogenic diets can do the same in the other direction. A holistic approach to health involves diet AND exercise. The two are related.

Just as we would adapt a “normal” diet to support athletic activity by modifying carbohydrate consumption, we can modify a ketogenic diet. I would argue that we need to exercise as part of a ketogenic diet so that we can transition into a primarily anaerobic metabolism (that which is used to make ATP for high intensity exercise). We need it as part of any healthy lifestyle, but stick with me.

As previously stated, while keto-adapted we use fat for nearly all of our energy needs. The best way to maintain metabolic flexibility while keto-adapted is to periodically reintroduce carbs. The exercise creates the stimulus for those carbs to be used rather than stored. We train the metabolism to have duality, and we have no negative effects of carbs (such as fat storage, extended elevations in insulin/glucose, etc.).

For the athletes, or the physically active with performance goals, the inverse is true. The exercise isn’t necessary to manage the carbohydrates and metabolic flexibility, the carbs are necessary to support performance. They are the only fuel source that can be used to support high-intensity activity, and athletes need to train at high intensity.

What is the solution to this keto-carb dilemma? Eat enough, but not too much. It’s the same as everything else really. We’re just at a different point on the spectrum than we thought. The best time to eat more carbohydrate is near exercise, so they go in and get burned up without having time to be stored. They are just energy molecules after all. Use the energy, and it won’t be stored.

For the complete scoop on dosing carbs while keto, and for the other 4 new rules, read my e-book, The New Rules of Keto. It is totally free. It is free because these are the things I want you to know. I think it’s vital to the growth of the low-carb movement and our ability as a species to improve our quality and quantity of life! If athletes and other active individuals need not avoid ketogenic diets, is there anyone who should? Find out in part 3!

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Macrophages and Energy Metabolism in Cancer: The Ketogenic Connection

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macrophages, keto diets and cancer

The notion that diet plays a pivotal role in the regulation of metabolic syndromes such as chronic inflammation has gained such wide acceptance that we now find the once accepted food pyramid established decades ago where fats and meats occupied a small percentage of total daily food intake is now replaced by one where carbohydrate intake has been dramatically reduced. Depending on the type of diet you are following, you may be consuming little to no carbohydrates and sugars, fruits and/or vegetables. You may also be consuming a high amount of animal protein from meats and/or fish, or your diet could comprise of mostly fats, as in the case of ketogenic (keto) diets.

The Ketogenic Diet is a high-fat/low-carbohydrate/adequate-protein diet. It has gained tremendous popularity because of proven anti-inflammatory actions via the suppression of glucose utilization. It has yielded impressive results in treatments for neuropathic pain, brain inflammation, or even weight loss accomplished via various mechanisms yet to be confirmed [1, 2, 3]. The ketogenic diet has been used since 1920 at John Hopkins to manage epilepsy in children. Recently, the ketogenic diet has been discovered to be effective against tumorigenesis in various cancer therapies [4]. It is believed to be effective against tumor progression because it is able to target the Warburg effect where cancer cells, in contrast to normal cells, mainly use aerobic glycolysis instead of oxidative phosphorylation (OXPHOS) in mitochondria to produce lactate. Lactate is the main energy substrate used by cancer cells for immune suppression and pH manipulation [28]. In an environment where circulating glucose levels are reduced under ketosis, cancer cells are hypothetically ‘starved’ of energy and unable to utilize lactate, while normal cells switch their metabolism to ketones generated by the ketogenic diet [5].

In preclinical evidence documenting the effects of ketogenic diets on tumor growth and progression, however, the association between ketogenic diets and tumorigenesis was not as straightforward as originally postulated. Data from multiple studies showed a range of effects on tumor growth. In some studies, the keto diet was anti-tumor, while in others there was no effect. In some cases, severe side effects or even pro-tumor effects resulted. It appears that whether the keto diet works or not depends upon the type of tumor being investigated and how the immune system responds to the diet. The best results were achieved in glioblastoma, and the worst in kidney cancer with a 50/50 outcome of pro-tumor/severe side effects. Melanoma treated with ketogenic diet also produced a 50/50 outcome of pro-tumor/no effect [5].

From Food to ATP: Understanding Mitochondrial Energetics and Cancer

When we eat different foods, they are broken down into smaller molecules like glucose, proteins and lipids before our cells can use them as fuel for energy, or as substrates for other molecules. When glucose is metabolized for fuel in our body, it is first converted into pyruvate in the cytosol, the liquid matrix within cell membranes. The classic view of pyruvate follows two paths: when there is a lack of oxygen, our body turns pyruvate into ATP via fermentation in the process of glycolysis. In the presence of oxygen, pyruvate enters the mitochondria and undergoes oxidative phosphorylation (OXPHOS) to create ATP.  Ketogenic diets supply our body with foods high in fats. Fatty acids are converted into acetyl-CoA in the mitochondria and undergo oxidative phosphorylation to create ATP.  Neither fatty acids nor protein undergo glycolysis directly in the generation of energy [15].

Cancer cells mostly derive their energy from glucose via glycolysis in the presence of oxygen. This unusual preference was first observed in 1956 by Otto Warburg who called this effect aerobic glycolysis, or what is now known ubiquitously as the Warburg Effect. Cancer cells thrive due to their ability to flexibly adapt their metabolism to increase their proliferation rate in the face of changing environments. The Warburg Effect refers to the unique trait of cancer cells to select glycolysis even in the presence of ample oxygen. This process of glycolysis used by cancer cells takes place in the cytosol of cells, where glucose is turned into pyruvate to yield ATP (energy). The process of glycolysis also results in the generation of nicotinamide adenine dinucleotide (NAD) in its reduced form NADH, as well as lactate [25]. How cancer cells manipulate these two important substrates to their advantage will be discussed later.

It is accepted that glycolysis yields two molecules of ATP per glucose molecule, and oxidative phosphorylation yields up to 38 molecules of ATP per glucose molecule. Whereas depending on the type of fatty acid, fatty acid oxidation can yield over 100 ATP molecules per fatty acid. The incorporation of ketogenic diet to curtail the growth of tumors seems like an excellent strategy, as it could sidestep the Warburg Effect, while providing ample units of cellular energy. However, fatty acid oxidation in the ketogenic diet also initiates an immune response, one that can be either pro- or anti-inflammatory, or both.

Ketogenesis, Inflammation, and Cancer

One of the main attractions of the ketogenic diet is the ability to reduce the symptoms or even reverse chronic inflammatory diseases. Injury triggers inflammatory responses, and recovery is the successful healing conclusion achieved via anti-inflammatory responses. Chronic inflammatory diseases are basically the result in the failure to resolve initial inflammatory responses. The traditional understanding is that glycolysis drives inflammation, and fatty acid oxidation (FAO) is always anti-inflammatory. In general, non-resolving inflammation in a tumor microenvironment is the hallmark of cancer [26]. In fact, classic healing cycles begin with injury and end with recovery [27] .  Proinflammatory responses are associated with enhanced glycolytic activity and breakdown of the mitochondrial tricarboxylic acid cycle (TCA). Hence, ketogenic diet is considered anti-inflammatory because it mainly uses fatty acid oxidation in the generation of energy in the mitochondria without the involvement of glycolysis [7].

Macrophage Metabolism, Inflammation, and Tumorigenesis

An interesting ongoing development in the study of immunology is the role played by intracellular metabolism as the regulator of the fate and function of cells of the immune system. The latest studies are now focused on how the polarization of macrophages and the modulation of their properties are affected by energy metabolism[22]. Macrophages are phagocytic cells present in almost all tissues. Macrophages are produced from bone marrow-derived blood monocytes, and are very much a part of our innate immune system. Macrophages play an important role in the initiation and resolution of inflammation. Depending on the signals they receive, macrophages can be pro-inflammatory, classified as M1, or anti-inflammatory, classified as M2. In cancer, macrophages can both increase and decrease tumor growth depending upon the type of tumor and type of macrophage involved. Interestingly, diet plays a role in determining the type of macrophage likely to be activated. There are two types of macrophages.

  • M1 macrophage metabolism is characterized by glycolysis, the pathway associated with cancer and often with the consumption of high carbohydrate diets. M1 macrophages have been associated with high levels of pro-inflammatory cytokines such as IL6, IL12, IL23, and tumor necrosis factor-α (TNF-α). M1 macrophages are able to produce substantial levels of reactive oxygen and nitrogen species, and are therefore, highly microbicidal and tumoricidal. Mitochondrial reactive oxygen species (mROS) are the key regulators of these M1 classically activated macrophages [8].
  • Conversely, M2 macrophage metabolism is characterized by fatty acid oxidation, producing ATP (energy) via oxidative phosphorylation. Unlike M1, M2 macrophages are associated with anti-inflammatory, tissue repair and resolution of inflammation, and are classified as alternatively activated macrophages. M2 macrophages are activated by Th2 cytokines like interleukin IL-4, IL-10, and IL-13 [9].

Recent research has discovered that these metabolic pathways are closely interconnected. Any attempt to define glycolysis as pro-inflammatory or fatty acid oxidation (FAO) as anti-inflammatory may be an oversimplification. Studies now demonstrate the need for glucose metabolism in anti-inflammatory as well as inflammatory macrophages, and that fatty acid oxidation (FAO) supports not only anti-inflammatory responses but also drives the activation of inflammatory macrophages [8].

M1 macrophages, being ‘pro-inflammatory’ are now identified as critical components involved in anti-tumor immunity, whereas M2, the macrophages traditionally viewed as anti-inflammatory, are now associated with tumor growth responses. Research now demonstrates that the infiltration of M2 macrophages can account for more than 50% of the tumor mass in some cancers. M2 type macrophages aid in metastasis by inducing angiogenesis (the development of new blood vessels), and the presence of M2 macrophage usually signify a poor prognosis for cancer survival. These macrophages that migrate to tumor sites and aid in angiogenesis and metastasis are called tumor-associated macrophages (TAMs) and they express a distinct M2 phenotype [10].

The Role of the Ketogenic Diet in Cancer

Two fundamental keys to understanding how the ketogenic diet affects tumorigenesis are the NADH:NAD+ ratio, and the access to lactate.

Lactate and Cancer

Cancer cells rely on glycolysis for energy even in the presence of oxygen, forsaking increased ATP energy production via oxidative phosphorylation (OXPHOS) in the mitochondria, in exchange for just 2 molecules of ATP and lactate. Lactate is a critical substrate for cancer cells, because it is used to generate lactic acid. Cancer cells remove one proton (H+) from lactate to produce lactic acid. Lactic acid produced by cancer cells has been found to play critical roles in their growth and proliferation. Cancer cells use lactic acid as an immunosuppressant as well as the promoter for angiogenesis, cell migration and metastasis. Lactic acid is also used by cancer cells to change the phenotype of M1 macrophages into the tumor-associated macrophage M2 [20, 21].

The level of lactate in tumor cells has been found to be highly correlated to the malignancy of tumors. Researchers discovered that some of the most malignant tumor lines tested were the ones that yielded the highest concentrations of lactate. Lactic acid produced by tumor cells during glycolysis is capable of generating signals that can induce the expression of the potent angiogenic factor Vascular Endothelial Growth Factor (VEGF) and the M2-like polarization of tumor-associated macrophages (TAMs) [21]. In addition, lactic acid from tumor cells has been found to inhibit pro-inflammatory cytokines, and the activation of T-cells.

“Lactic acid suppressed the proliferation and cytokine production of human cytotoxic T lymphocytes (CTLs) up to 95% and led to a 50% decrease in cytotoxic activity” [32].

Ketones and Lactate: A Misunderstood Relationship

The main premise for using Keto diets in cancer therapies is its ability to simulate the natural state of fasting, where the body breaks down stored body fat to produce ketones for energy when food is not available. Hypothetically, the burning of fats in Keto diets will reduce the flux of glucose through glycolytic pathways that are favored by cancer cells in the generation of energy and critical substrates like lactate [29].

We already know that lactate is an important substrate for cancer cells. But how effective are Keto diets in suppressing lactate formation? One would think that since glucose consumption is significantly reduced in Keto diets, lactate production levels should also decline.

Let us take a look at glioblastoma, where Keto diets have been reported to have a high success rate. Our brains are able to use ketones as fuel. Keto diets can supply adequate fuel to our brains via ketones when glucose is not available. Keeping the level of blood glucose low may sound quite attractive as it has been reported that “hyperglycemia is associated with adverse prognosis and postoperative function loss in GBM (glioblastoma multiforme) patients” [30]. Does that mean that if one can artificially reduce blood sugar levels by implementing Keto diets, the prognosis for glioblastoma patients will improve? The answer may surprise you, but not if you understand that lactate is also an important substrate for cell survival in normal non-cancerous cells.

A study on the effects of low carbohydrate/high fat diets and high carbohydrate/low fat diets in ultra-endurance athletes revealed that plasma glucose and serum insulin were not significantly different between the two groups when they were at rest and also during exercise. There was no significant difference between the two groups in insulin resistance as determined by HOMA (a homeostatic model assessment of beta cell function and insulin resistance). However, serum lactate increased by twofold during the last hour of exercise training in the group of athletes consuming a low carbohydrate/high fat diet. The researchers found that all athletes in the low carbohydrate/high fat group broke down substantially more glycogen in their muscles than the total amount of carbohydrate oxidized during the 3 hour run. Why were muscles broken down for glycogen when substrates like fatty acids were readily available to the athletes on Keto diets? Obviously these glycogen were not used for energy production because they were not oxidized. The researchers believed the glycogen were a necessary source for the production of lactate [31].

Our bodies are very adept at maintaining homeostasis. When glucose availability is limited by diet, our bodies can produce glucose from other sources like proteins and fatty acids. Gluconeogenesis is one of several main mechanisms used by humans and many other animals to maintain blood glucose levels.  Gluconeogenesis uses non-carbohydrate substrates from lipids such as triglycerides to produce glucose in the liver [19]. Amino acids from protein, such as the glucogenic amino acids can also be converted into glucose through gluconeogenesis [18].

It is highly likely that the long-term consumption of a low-carbohydrate/high-fat diet leads to adaptations in our body to maintain homeostasis in the regulation of glycogen so as to preserve an environment that is similar to one maintained under high carbohydrate consumption [31]. Based upon these findings, it is perhaps necessary to re-examine the ability of the Keto diet to truly reduce access to lactate in cancer cells.

Is NAD+ the Double-edged Sword in Ketogenic Diets?

In recent years, NAD+ has been recognized as having neuroprotective qualities in addition to anti-inflammatory and anti-aging benefits [34].

NAD, or Nicotinamide adenine dinucleotide (NAD) is a coenzyme found in all living cells. It exists in two forms, NAD+, the oxidized form, and NADH, the reduced form. The main functions of NAD is to transfer electrons.  NAD+ accepts electrons from other molecules to produce NADH, which then can donate electrons again to other molecules [24].

In the process of glycolysis, electrons are added to NAD+, resulting in the reduced form of NADH. Two molecules of NADH are formed per molecule of glucose during glycolysis. During oxidative phosphorylation (OXPHOS) these NADH molecules donate their electrons to form NAD+, which can then be used again for glycolysis [15]. When the metabolic pathways used is predominantly glycolytic, there will be an NADH excess because more NAD+ are consumed in the process.

A high NADH:NAD+ ratio in the cytosol is an indication of high glycolytic activity. Higher levels of NADH results in an increase of pro-inflammatory gene expression of macrophages with the M1 phenotype. Conversely, limited glucose availability as a result of diet restrictions can lower the NADH:NAD+ ratio. When there is more NAD+ to NADH, pro-inflammatory gene expression and responses are suppressed as a consequence [16].

Ketogenic diets are believed to be able to increase NAD+.  Ketogenic diets have been found to significantly raise hippocampal NAD+ levels in studies on rodents, conferring neuroprotective benefits [17]. Having more NAD+ than NADH also leads to the suppression of glycolysis, which in turn will increase anti-inflammatory macrophage responses that can reduce brain inflammation, tissue loss, and functional impairment after brain injury [16]. In terms of understanding how the NADH:NAD+ ratio relates to the two macrophage phenotypes, a simple way is to remember that:

  • Low NADH, high NAD+ = Anti-inflammatory, tumor-promoting macrophage (M2)
  • High NADH, low NAD+ = Pro-inflammatory, tumor-suppressing macrophage (M1)

A low NADH:NAD+ ratio (low level of NADH but high level of NAD+) is pro-tumor. Cancer cells thrive when there is an abundance of NAD+.  NAD+ is an essential coenzyme for aerobic glycolysis. A higher rate of glycolysis will reduce the amount of NAD+ available. Fewer NAD+ in turn slows down the rate of aerobic glycolysis. So the more cancer cells rely on glycolysis, the more NAD+ they require. It has been demonstrated that NAD+ levels are much higher in cancer cells compared to normal cells, likely due to an upregulation of NAD+ synthesis by cancer cells, [33] and the inhibition of the NAD+ metabolic pathways leads to enhanced autophagy and decreased survival rate of cancer cells [35].  When one employs a high fat diet to inhibit cancer growth via the limitation of access to glucose, the inadvertent generation of NAD+ is a factor that must be taken into consideration.

The Future of Macrophage Polarization

Cancer cells are able to circumvent our body’s natural immune defenses via many mechanisms. By manipulating lactate produced during aerobic glycolysis, lactic acid is used by cancer cells to induce the polarization of macrophage into the tumor-associated macrophage with distinct M2 phenotypes for growth and proliferation, chemotherapeutic resistance and immune evasion[37]. Ketogenic diets may limit the substrates available to tumors for use in glycolysis, but they are not able to suppress all the tactics used by cancer cells to create environments that are hospitable to their proliferation.

The type of diet we choose exerts significant influence on how macrophages are activated in our body. Depending on their activation status, macrophages can either facilitate tumorigenesis by antagonizing the cytotoxic activity of immune cells or suppress tumor progression by enhancing anti-tumor responses. Current strategies in the fight against cancer development show promise in the manipulation of macrophage responses via therapies that either block the recruitment or depletion of macrophages from the tumor; affect the polarization of the tumor-associated macrophage to an anti-tumorigenic phenotype; or the reactivation of immunostimulation[36]. Whichever therapy is employed in the manipulation of macrophage polarization, the incorporation of energy metabolism as part of the strategy may prove truly invaluable.

References

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  26. Targeting Inflammation in Cancer Prevention and Therapy http://cancerpreventionresearch.aacrjournals.org/content/9/12/895.full-text.pdf
  27. Metabolic features and regulation of the healing cycle—A new model for chronic disease pathogenesis and treatmenthttps://www.sciencedirect.com/science/article/pii/S1567724918301053?via%3Dihub
  28. Cancer-generated lactic acid: a regulatory, immunosuppressive metabolite https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3757307/
  29. Ketogenic diets as an adjuvant therapy in glioblastoma (the KEATING trial): study protocol for a randomized pilot study https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5704454/
  30. Investigating the Ketogenic Diet As Treatment for Primary Aggressive Brain Cancer: Challenges and Lessons Learned https://www.frontiersin.org/articles/10.3389/fnut.2018.00011/full 
  31. Metabolic characteristics of keto-adapted ultra-endurance runners.https://www.ncbi.nlm.nih.gov/pubmed/26892521 
  32. Inhibitory effect of tumor cell–derived lactic acid on human T cells https://www.ncbi.nlm.nih.gov/pubmed/17255361 
  33. NAD+ salvage pathway in cancer metabolism and therapy https://www.sciencedirect.com/science/article/abs/pii/S1043661816311434 
  34. NAD+ in aging, metabolism, and neurodegeneration http://science.sciencemag.org/content/350/6265/1208 
  35. The NAD+ salvage pathway modulates cancer cell viability via p73  https://www.nature.com/articles/cdd2015134 
  36. Macrophages as Key Drivers of Cancer Progression and Metastasis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5292164/ 
  37. Tumor-associated macrophages: implications in cancer immunotherapy https://www.futuremedicine.com/doi/abs/10.2217/imt-2016-0135?src=recsys&journalCode=imt

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Nutritional Ketosis 101: A Personal Account

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Ketosis Urine Strip

Carrying a lot of excess bodily “cargo,” I decided to embark upon a bifurcated journey of nutritional ketosis, or keto for short. First, I seek to lose at least 20 percent of my body weight. Second, I want to compare my pre-ketosis blood test results — specifically the lipid panel — with the values after being in nutritional ketosis.

What is Nutritional Ketosis?

In short, nutritional ketosis is the metabolic state of burning fat while on a low-carbohydrate, moderate-protein, high-fat diet. The words “high fat” usually conjure a vision of the cardiovascular system laden with animal fats. But this is mistaken because mainstream medicine and news outlets equate “high fat” to high cholesterol, and believe high cholesterol heightens the risk of heart disease. Nothing could be further from the truth.

Consuming healthy saturated and non-saturated fat as part of a ketogenic diet makes the body feel great. Health benefits include: effective weight loss and maintenance; satiety; stabilized blood sugar and restored insulin sensitivity; and eliminated heartburn to name a few. Furthermore, my blood lipid panel values — cholesterols and triglycerides –- plummeted after keeping keto for about two weeks! My physician exclaimed, “Impressive!”

Scientific research including rigorous preclinical and clinical studies indicates that a ketogenic diet offers “a promising and powerful option for adjuvant therapy for a range of cancers.” For example, University researchers in Salzburg, Austria concluded in the February 2018 issue the journal Aging that a ketogenic diet induces ketosis that can starve cancer cells of energy while normal cells use their ketone bodies to survive. In addition, the reduction of blood glucose normalizes insulin, resulting in less fuel for cancer cells.

How Do I Enter Ketosis?

A ketogenic diet burns fat; whereas, high carbohydrate consumption burns sugar, usually not getting past the stores of glucose to achieve the state of burning fat. We know that many diets are replete with carbohydrates – bread, pasta, rice, sugar, cereal, processed foods – and, many people (including me) who ingest those carbs are waddling around wondering how they became overweight or obese. (I endeavor to become a former overweight person.)

Simply stated, get all sugar out of your diet. In today’s world eschewing sugar presents a daily challenge, given hidden sugars lurking in processed foods including dressings and sauces. Sugar is almost everywhere! But there are ways to eliminate it from your daily diet.

So, what can you eat? Mainly foods high in fat. Such as bacon, egg yolks, beef, and sausage. Also healthy fats such as avocado, coconut oil, extra virgin olive oil, and organic butter.

I understand that many of these foods are perceived as “no no’s” in our diets. However, they are necessary to achieve and maintain ketosis—to enjoy a healthier and slimmer life.

How Do I Test for Nutritional Ketosis?

Ketones, fuel for our mitochondria, are the overall product of nutritional ketosis for which testing can be easy, relatively inexpensive, and private.

The most common ketosis test involves urinating on a disposable strip containing a small chemical pad to detect the level of acetoacetate (AcAc) – the primary ketone body in urine. Another test can be performed at home by measuring beta-hydroxybutyrate (BHB) in the blood. A third way of evaluating ketones entails using a breathing device to measure acetone, the main ketone body in the breath.

Ketosis Versus Ketoacidosis

It is imperative to understand that when maintaining your blood sugar level in the normal range (less than 100 mg/dL) and producing insulin, the presence of ketosis is not harmful! However, if you encounter any doubters, including medical professionals, who claim that nutritional ketosis is unhealthy, see if they have confused “ketosis” with “ketoacidosis”.

Ketoacidosis occurs in diabetics who have both high blood glucose (greater than 240 mg/dL) and elevated blood ketone values (greater than 10 mill molar/L). Diabetic ketoacidosis occurs primarily in Type 1 diabetics who cannot produce insulin. Some Type 2 diabetics who have excess blood sugar and blood ketones as well as dependence on insulin also need to beware of ketoacidosis.

How Do I Attain My Ketosis Goals?

Often referred to as the father of medicine, Hippocrates wisely stated,

“If we could give every individual the right amount of nourishment and exercise, not too little and not too much, we would have found the safest way to health.”

Based on my recent experience with ketosis and moderate exercise (a rowing machine), I may have found the “sweet spot”: 1) steadily losing weight and inches, 2) feeling healthy and satiated, and 3) attaining and maintaining healthy cholesterol and triglycerides. And I am confident that my risk of cancer as well as a long list of medical conditions is being reduced as I enjoy delicious food and healthy exercise.

I penned this article with the intention of presenting the reader a brief introduction to a nutritional ketogenic diet. For additional information, I recommend consulting ketogenic diet books including:

  • Keto Clarity. Moore with Eric C. Westman, MD. Victory Belt Publishing LLC. 2014.
  • The Obesity Code. Jason Fung, MD. Greystone Books. 2016.

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About the Author: Susan Rex Ryan enjoys research and writing about health as well as experiencing its amazing benefits. She authored the award-winning and perennial bestselling book called Defend Your Life about her journey with vitamin D3. Ms. Ryan recently wrote her second book called Silent Inheritance: Are You Predisposed to Depression about understanding depression and how to cope with it.

Visit Sue’s blog at smilinsuepubs.com for a plethora of health articles. Follow her on Facebook and Twitter @vitD3Sue.

© 2018 Smilin Sue Publishing, LLC. All rights reserved.

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The Ketogenic Diet: What You Need to Know

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Dietary Fat

There is hardly a day that passes without seeing a new article popping up about the damage sugar and refined carbs can cause but only lately is the connection of sugar to obesity and metabolic disorders starting to be realized. Many people we know may have some weight problems or metabolic health conditions and follow some weight loss program—none of which seems to be effective in the long run. This makes sense. If any weight loss program had led to permanent weight loss, those using it could stop and the company promoting it would go out of business. Long-term (often life-long) membership is essential if one wants to avoid yoyo dieting.

Lately, I see many people rushing to change from the Standard American Diet (SAD) to various new diets, such as the Low Carbs High Fat (LCHF) or the Ketogenic diets. Are all these “diets” for weight loss? Some people call these “fad” diets, but are they?

There was a time when sugar covered cereals were called “fads” but look what has become of that fad! It has become our everyday SAD. Fad is “a practice or interest followed for a time with exaggerated zeal: craze” (here). Sugar covered cereals have been with us for over 100 years, so definitely not a fad. What about the LCHF and the ketogenic Diets? Are they fads? Maybe, maybe not. Let’s dig a little deeper into the ketogenic diet since I consider the LCHF a less strict version of the ketogenic diet.

Is the Ketogenic Diet a Fad?

Looking at its history, “[ketogenic] dietary regimens have been used to treat epilepsy since at least 500 BC” (here). The ketogenic diet utilizes a metabolic process that can be awakened by fasting—though fasting is not necessary. “The ketogenic diet was introduced by modern physicians as a treatment for epilepsy in the 1920s” (here). Therefore, we can safely say it is not a fad. Since it has been used therapeutically for seizures for a very long time, it is not a diet either. What it this ketogenic “thing”?

Ketogenic Metabolic Process

Ketogenic is the human native metabolic process. It is a different metabolic process from the process SAD requires. The ketogenic diet is mostly fat, limited amount of protein, and very small amounts of carbohydrates—the exact opposite of SAD. Eating carbohydrates or protein require insulin for conversion to glucose. Fat is the only macro-nutrient that doesn’t need insulin to generate ATP (Adenosine triphosphate)–in ketosis the role of insulin is fat regulation rather than glucose management to generate ATP (here). ATP is cellular energy, which, after all, is the goal of eating macro-nutrients.

Metabolic Processes

Image from Ketopia.

As you can see in the above image, the end-product for all metabolic processes is the same: energy. However, the complexity differs—this metabolism map is simplified. Note something very important: we can completely remove carbohydrates from the above diagram and not miss a beat in our energy creation. Protein only partially needs to be converted to glucose at the pyruvate step but some protein can directly turn into energy without conversion to glucose. We can remove all sugar, pasta, pizza, cereal, whole wheat bread, all fruits and vegetables from our diet and eat fat and protein instead to meet all our energy need. Most minerals and vitamins are found in meat and dairy so supplementation or eating fruits and veggies may not be necessary. Vitamin C is found in eggs and organ meats.

Why is Ketogenic Important?

Carbohydrates joined our evolutionary path several times, depending on how far you wish to go back. I choose to go back to just before farming. Prior to farming, carbohydrates were hard to come by, especially during the Ice Age. Even civilizations in hot parts of the world, such as the Masai in Africa, don’t eat carbohydrates because they have too little nutritional value. They eat meat, fat, milk, and blood—all high fat and nutrient-dense food. Carbohydrates are not nutrient dense since they lack many amino acids and fatty acids.

The ketogenic metabolic process, on the other hand, is rich in amino and fatty acids, minerals, and vitamins. See the chart below for vitamin and minerals and where we can find most of them.

nutrition in meat

Ketogenic is a simpler metabolic process that burns fat, so the belly you built up over the years can be used up as energy. Furthermore, since our brain is mostly made from fat, we might as well feed it fat. Feeding the brain fat is beneficial to your health in many ways. The ketogenic diet has been used therapeutically because of the high fat. It is used as curative today for epilepsy, cancer, type 2 diabetes, obesity, for neuromuscular diseases like Parkinson’s, Alzheimer’s, MS, sleep disorders and autism, and even migraines and much more. It appears that the ketogenic way of eating cures the negative consequences of the SAD diet.

Is Ketosis a Starvation Diet?

People often label ketosis, the method of fat burning in the ketogenic diet, a “starvation” diet. Some even call it a state of “acid-base disturbance” without realizing its importance. However, ketosis is far from being a state of starvation since our body has a lot more fat-storage ability than glucose (glycogen) storage at any given time. While our liver can retain maximum 500 grams of glucose equivalent in glycogen (about 2000 calories worth of energy), our body contains tens or hundreds of thousands of fat calories (depending on how much fat you carry). Should a famine ever arrive, the ones starving to death will be those who depend on the availability of carbohydrates and not those who can store and burn their fat.

We need to turn the “starvation” theory up-side-down. Carbohydrates (prior to our commercialization) were only available for short periods of time and only in some places where the climate was favorable. How did humans survive in cold climates or seasons? Eating fat and meat – of course – from the animals they captured.

How Can More Calories be Generated by Starvation?

From each gram of fat 9 calories of energy are generated, whereas from a gram of carbohydrates only 4 calories of energy is generated Which one is the starvation mode in your opinion? It seems that consuming carbohydrates makes sense only as a desperation move in times of fat shortages.

Note that if you eat only carbohydrates, you need to eat 2.25 times as much as when you eat fat since carbs only generate 4 Calories whereas fat 9 (simple math). I would think that a starvation diet becomes necessary when nothing better is available. In this case, carbohydrates offer less than half the energy so that is indeed the starvation diet. Furthermore, the length of time one needs to eat also matters. Surviving on carbohydrates takes 2.25 times as long eating-time as surviving on fat if we want to eat the same amount in calories. This translates very well to our modern society where eating three main meals and two snacks is necessary to survive on a carbohydrate rich SAD diet while those on the ketogenic diet may eat only once a day to get the same calories (this is because of the calorie differences macro-nutrient types provide). Since the ketogenic diet is so much more advantageous, let’s evaluate some common beliefs about it.

Keto Flu

Keto flu is not an illness. It represents a transition time for your body from carbohydrate to fat burning mode. It requires the cooperation of many hormones and the replacement of some cells since these metabolic processes are extremely different. During this initial period you don’t burn fat efficiently, you may feel more tired during workout, have a headache, cramps, or bad breath. This period may last anywhere from a couple of days to several months. It does dissipate, however, but most academic research has been conducted for too short a time period for the keto flu to pass and much fight is ongoing to prove that. The subject is still only discussed within academic circles.

Individuals who try the ketogenic diet have little support from their doctors and nutritionists, most of whom have never heard of the ketogenic diet because they must follow the dietary guidelines of the USDA or the American Heart Association. As a result, people must rely on the often inaccurate ketogenic material found on the Internet, as this dieter explains.

Useful Ketogenic Information

Ketogenic diet is inhospitable to most parasitic and bacterial life in the human body (here). Bacterial infections, yeast and perhaps even mold find it impossible to survive in an environment that uses fat rather than glucose for metabolism (here). Cancer is a metabolic disease that feeds on glucose (here). Where there is no glucose (or a very limited amount), there is a much smaller likelihood of cancer–cancer is a metabolic disease (here).

My Experiences with Dairy

Whole milk doesn’t affect ketosis . Whole milk has no sugar (in spite of the label on the box). It has lactose. Lactose is a disaccharide, meaning two molecules are bonded: glucose and galactose. Lactose requires the enzyme lactase to break it up and this happens in the intestines. Therefore, the sugar from milk doesn’t increase in the blood until the enzymes have broken lactose into glucose and galactose (here). Since lactose is a disaccharide bond between glucose and galactose, only 50% of it is glucose. While glucose certainly finds its way back to the blood from the intestines, it does so slowly and perhaps some happy bacteria already fermented some of it. So, even the assumption of 50% returning as glucose is very generous.

Lactose free milk affects your glucose levels immediately because in this type of milk the lactose is already broken up into the simple sugars of glucose and galactose (here). Don’t drink lactose free milk in ketosis.

Yogurt interferes with ketosis because of the fermenting of lactose by the bacterial cultures produce lactic acid (here). This means that much of the lactose bonds have been broken before you put yogurt into your mouth. Yogurt will likely bring you out of ketosis—depending on how much glucose is left unfermented in it.

Medicines, Supplements, and Ketosis

Prescription medicines as well as some supplements may interfere with ketosis (here). This is rarely if ever talked about but I can pass on my experience. Many medicines and supplements use insulin receptors to get into our cells. A notorious prescription medicine to instantly bring you out of ketosis is Prednisone—including corticosteroid epidurals. Prednisone uses up all the insulin your body is capable to produce (it can induce type 2 diabetes) and starve the brain of glucose (some brain parts always need glucose though small amounts). The more the brain demands glucose, the more glycogen the liver pumps into the blood but as there are no free insulin receptors, blood sugar levels may reach near diabetic level (mine did from Prednisone).

Some vitamins, such as vitamins D and C also use insulin receptors and you may find similar behavior to Prednisone (here). Some medicines may work against ketosis. The ketogenic diet works best in a medicine free body because this “diet and nutritional supplements improve so many conditions that the prescriptions often become an overdose or unnecessarily strong” (here). Furthermore, Western Medicines are made to work in a carbs-burning metabolic process so it is not at all surprising that they don’t work in a fat burning metabolism.

For example, some seizure or heart arrhythmia medications may become agonists in a ketogenic metabolic process. Ketosis is a state when your body is in recovery mode, rebuilding fat and cholesterol in your brain and heart to insulate your voltage passing neurons. Medicines that block these neurons from working, such as voltage gated calcium channel blockers or voltage gated sodium-potassium pumps or channels blockers, may end up amplifying the  condition by working against the medicine while the medicine is working against the ketogenic repair process—this happened to me.

A person should not come in and out of ketosis. One is either in the ketogenic metabolic mode or out. A body can only have one metabolic process at a time given that both processes use insulin but for very different purpose–as described earlier. When a body is not used to eating carbohydrates, the insulin resets to a healthy level. This means that the reaction to a cheat day may bring with it a diabetic level insulin spike. Repeat this often and this may become a factor in insulin resistance that perhaps nothing can reverse. So make a decision and stick with it. As my body proved it to me (and to a few others in the ketogenic mild for migraine group on Facebook), once the body is in efficient fat-burning mode, it wants to stay there.

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Hormones Matter needs funding now. Our research funding was cut recently and because of our commitment to independent health research and journalism, unbiased by commercial interests, we allow minimal advertising on the site. That means all funding must come from you, our readers. Don’t let Hormones Matter die.

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keto basicsKeto Dieting: Understanding the Basics

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