By Jay Feldman, Health Coach
First a quick note from CA: there are many spiritual benefits of fasting beyond the health benefits. I still think fasting is an important religious practice and FU to a modern society that preaches mindless consumption. In this article below, Jay is specifically referring to the health and metabolic effects of fasting. Okay, now onto the good stuff…..
Fasting may very well have been an involuntary hardship of our evolutionary journey.
And it may very well have been “natural” or in line with our “ancestral way of eating,” and assuming it was, it certainly would have been something that we had adapted to.
But does that mean that fasting improves our health?
While the suggestion that “fasting is beneficial because it was part of our evolutionary history” may sound like a far cry from the reductionistic, mechanical view of the human body embodied by conventional medicine, it actually comes from the exact same mindset.
The idea portrayed here is that that fasting is beneficial because we were programmed for it, where only those with the genetic makeup fit for fasting would have survived. And now, the machine or computer that is our body must follow this genetic programming in order to remain healthy.
But the problem here is that we’re not pre-programmed machines!
Instead, we constantly adapt to the diverse, ever-changing environments around us, which fasting would likely have been a part of.
And in order to determine whether fasting is something we would want to adapt to and would support our health, we have to dig below the surface-level naturalistic arguments in favor of fasting and evaluate what happens on a physiological level when we fast.
To begin, we know that fasting is characterized by a single quality: not eating for a period of time. And when we don’t eat for a period of time, there are several physiological effects to consider.
It All Starts With Blood Sugar
These effects begin with our blood sugar.
Our blood sugar is one of the main interfaces our bodies use to sense the energetic availability of our environment, and for good reason.
Our brains need sugar as a fuel, but they can’t store any so that sugar must be supplied by the blood. And, as our most energy intensive organ (making up 20-25% of our total energy requirements), our brains require quite a bit of sugar (1).
(Yes, some of this energy can be supplied by ketones, but we’ll get there in a moment.)
So, it’s vitally important that our blood contains enough sugar to supply fuel for the brain, otherwise our brain wouldn’t function and neither would we!
When we eat carbohydrates, some amount of those carbohydrates ends up entering the blood as glucose, which raises our blood sugar and supplies fuel to the brain and other organs.
But when we stop eating carbohydrates (whether we’re on a low-carb diet or we’re fasting), there aren’t any carbohydrates available to supply our blood sugar, and our blood sugar begins to drop as the glucose gets used as fuel.
Now because adequate blood sugar levels are so vitally important, there’s a cascade of adaptive mechanisms in place to help to raise our blood sugar when it drops, which involves the release of stress hormones glucagon, epinephrine (adrenaline), growth hormone, and cortisol (2).
These hormones have several stepwise effects, depending on the severity and duration of the drop in blood sugar, that help to maintain blood sugar and conserve glucose:
- They increase glucose production at the liver by encouraging the breakdown of glycogen, the body’s stored form of sugar
- They switch the body’s primary fuel from sugar to fat, evidenced by an increase in the release of free fatty acids via lipolysis
- They trigger the conversion of amino acids, either from the protein in the food we’re eating or from muscles, organs, or other tissues, to glucose through a process called gluconeogenesis
- They stimulate ketone production to supplement glucose as a fuel for the brain
So to summarize, when we’re not maintaining our blood sugar by eating carbohydrates, it must be maintained by the stress hormones glucagon, epinephrine, growth hormone, and cortisol.
The problem here is that relying on these stress hormones comes at a cost.
As I mentioned earlier, our blood sugar is used as a barometer for the energetic availability of our environment. So when these stress hormones are elevated, it’s a sign that our environment isn’t supplying enough high-quality fuel to meet our energetic needs.
As a result, these stress hormones will decrease our metabolism by downregulating several processes, including:
- The function of our immune system, reproductive system, cognitive capacity and nervous system, and digestive system (3, 4, 5, 6, 7, 8, 9, 10, 11, 12)
- The production of thyroid hormones (4, 13, 14)
- The conversion of T4 (the inactive thyroid hormone) to T3 (the active thyroid hormone) (13, 14 15, 16, 17, 18)
- The prometabolic reproductive hormones (4, 19)
With these effects in mind, it’s no surprise that these stress hormones are implicated in diabetes, obesity, heart disease, osteoporosis, depression, and many other chronic diseases.
Now we know that when we fast we abstain from carbohydrates, so our blood sugar must be maintained by the effects of the stress hormones. So, it’s no surprise that fasting has been shown to be quite stressful and cause the same increases in stress hormones and reduction in thyroid activity and metabolism (20, 21, 22):
“The overall result of these complex axis changes in various tissues during fasting is downregulation of the axis, which is assumed to represent an energy-saving mechanism, instrumental in times of food shortage.” (20)
But, it doesn’t end there.
When relying on gluconeogenesis, our bodies will prefer to use the amino acids from the protein we’re eating. But when we fast we also abstain from eating protein, so our bodies must break down their own muscles, organs, and other tissues to supply the amino acids for glucose production, which ends up leading to muscle wasting while fasting! (23)
And remember, our blood sugar is only the first interface that reflects the response to fasting. The elevated stress hormones then go on to downregulate all of our higher-level metabolic mediators, from our thyroid to our reproductive hormones, as a cohesive response to downregulate our metabolic function.
The Fasting-Insulin Theory of Obesity
But what about insulin? Isn’t fasting supposed to decrease insulin, and doesn’t insulin cause chronic diseases?
Well, yes and no.
Yes, just like any period of carb restriction (including low-carb and keto diets), fasting does decrease insulin.
But no, that’s not inherently a good thing and insulin is not responsible for all (or any) chronic diseases.
Insulin has gotten a bad rap, much like cholesterol in the case of heart disease.
Remember the idea that you wouldn’t blame firemen for a fire, so it wouldn’t make sense to blame cholesterol for heart disease?
Well, the same rings true for insulin and diabetes and obesity.
Insulin doesn’t cause these conditions just because it’s found to be elevated in those who have them.
Insulin acts as a signal to help glucose get into the cell and is released when our blood sugar is elevated. Normally, the glucose from the blood will then enter the tissues where it’s used to produce energy and insulin then decreases.
But in these chronic disease states, the cells aren’t effectively converting that glucose to energy, leading to a buildup of glucose in the cells. This then prevents the glucose in the blood from entering the tissues, leading to increased blood sugar and increased insulin (24, 25, 26, 27).
This is considered insulin resistance, which is a bit of a misnomer considering the underlying issue is actually inefficient glucose metabolism, not elevated insulin or an inability to respond to insulin.
In an insulin resistant state, the stress hormones are also elevated due to the lack of energy. These stress hormones drive fat storage and slow metabolism while also stimulating gluconeogenesis, leading to the typical presentation of fasting hyperglycemia (25, 28, 29, 30).
And, these effects all make perfect sense in the adaptive context.
The inhibition of efficient glucose metabolism in insulin resistance acts as a signal of a suboptimal environment, as anything that’s stressful can cause this effect (including infections, PUFA, and the stress hormones themselves).
In this manner, this insulin resistant state acts as a part of a protective mechanism to conserve energy and fuel by slowing the metabolism and increasing the storage of food as fat, as is mediated by the hormones we’ve discussed.
Now you may also be surprised to know that fasting actually induces insulin resistance directly!
This falls directly in line with the physiological mechanisms we’ve discussed, as we know that fasting is stressful, slows thyroid activity, and reduces metabolism. And, we know that this insulin resistance is simply a symptom of stress that allows for adaptations that further the conservation of energy.
All of this is acknowledged in the following quote:
“Hepatic- and skeletal muscle-cell insulin resistance is induced in numerous contexts including the elevated levels of fatty-acid oxidation induced via hypo-caloric feeding, fasting, or starvation (Newman and Brodows, 1983; Björkman and Eriksson, 1985; Cigolini et al., 1985; Svanfeldt et al., 2003). This cooperative strategy diverts nutrient-energy substrates to other cells (e.g., neurons), and allows for the survival of all cells in the body. As we posited previously, the naturally occurring insulin resistance of pregnancy is a cooperative strategy that drives nutrient-energy to the fetus (Archer, 2015c; Archer and McDonald, 2017; Archer et al., 2018). Thus, in contrast to the current consensus on the pathological nature of insulin resistance, we posit that insulin resistance is an essential feature of mammalian metabolism, and our frameworks of competitive and cooperative strategies explain the evolutionary benefits of this cooperative strategy in the mammalian ecosystem.” (31)
In other words, the goal of decreasing insulin through fasting ends up raising the stress hormones and causing insulin resistance!
But perhaps counterintuitively, and in contrast to the insulin resistance induced by fasting, increasing carbohydrate intake and stimulating insulin actually ends up increasing insulin sensitivity by decreasing the stress hormones and shifting away from stress-induced fat metabolism (
And, not coincidentally, increasing insulin and decreasing the stress hormones in this way doesn’t lead to fat gain as the carb-insulin model of obesity would posit, and instead supports body fat loss and the maintenance of lean body mass (40, 41, 42, 43, 44).
A Beloved Pastime Since The Dawn of Time
But wait a minute…
We’ve been fasting for thousands of years – it’s part of our evolutionary makeup! How could it not be beneficial!
It should really go without saying, but just because we did something for thousands of years doesn’t mean it’s optimal for our health.
Along the same line of reasoning, throughout our evolutionary history we didn’t live in houses, wear shoes, go to gyms to lift weights, or use refrigerators, so not doing those things would have to be beneficial too.
While this is a relatively surface-level argument, it does get at the main idea – just because we did something, or more precisely, just because we adapted to something, doesn’t mean it’s a good thing!
Rather, when it comes to adapting to stress, it always comes at a cost…
This brings us to a concept called hormesis, which is the idea that small amounts of stress lead to adaptations that make us stronger and healthier.
The idea sounds logical on the surface and is subscribed to by most in favor of fasting, and also comes in the form of interventions like ketogenic diets, cold thermogenesis or cryotherapy, and supplements like resveratrol.
While digging into the multitude of reasons why this concept is heavily flawed would take multiple articles of its own, the most important point to consider is that adapting to stress doesn’t make us stronger.
Stress occurs when the body’s energy demand exceeds its energy supply, and backup mechanisms are needed to supply energy (you’re already familiar with these mechanisms involving the stress hormones we discussed earlier).
Adapting to stress in this way causes us to conserve our energy in the long term to prepare for future stress.
And as we talked about earlier, this energy conservation means lower levels of function, almost like a step toward hibernation, where an organism prepares for extensive future stress by decreasing its function as much as possible to conserve energy and increase its chances of survival.
Along the way, this energy conservation also comes with degeneration, as the body no longer has the energy to properly maintain its structure.
Another way to think about it is that in any situation where we don’t have enough energy available, we have to borrow that energy from other areas through stress loans, which puts us in energy debt. Our bodies know that this is a slippery slope that could lead to bankruptcy, so they begin to cut costs to live within their energy means. As more loans are taken out and the debt accumulates, they cut more and more until they can only afford the bare essentials required to live.
And while this does help our bodies avoid bankruptcy, it’s certainly not an optimal or comfortable way to live.
In other words, the survival state that results from accumulated stress is clearly not the picture of vibrant health we’re looking to achieve!
Now it’s also necessary to point out that not all things that cause stress are harmful and drive us toward this hibernation survival state.
This isn’t because the stress magically changes to “good stress.” Rather, stimuli have effects other than their propensity to cause stress, and these other effects, called specific effects, can be beneficial enough to outweigh the stress.
Take exercise, for example.
We know that a moderate dose of exercise can increase our energy demands and cause stress. But at the same time, exercise puts tension on our musculofascial system in a way that has been shown to be universally beneficial.
At excessive levels of exercise, however, we see that the increased stress begins to outweigh the beneficial specific effects and we see adverse cardiovascular effects, decreased libido, intestinal permeability, liver and kidney damage, and various other indicators of increased damage and inflammation (45).
But while the type, intensity, and volume of exercise can all affect whether the specific effects will outweigh the stressor effects, there are some stimuli that have virtually no beneficial specific effects but cause stress (like mercury exposure, ionizing radiation, or a paper cut) and others that have beneficial specific effects and cause very little stress because they don’t demand much energy (like relaxing in the sun or reading an interesting book).
And that brings us back to the original question: what about fasting?
Fasting In The Short-Term: Gut Relief
But as we discussed, not everything that’s stressful is inherently harmful (like exercise), because we must also account for the specific effects of the stimulus. And in the case of fasting, the most noteworthy specific effects are gut relief and relief from inefficient glucose metabolism.
So, do these specific effects outweigh the stress?
In the short-term, the answer tends to be rather individual, depending on the impact of gut relief and relief from inefficient glucose metabolism
The effects of gut relief might sound trivial, but it can be a major factor affecting our health.
Endotoxin (also known as LPS or lipopolysaccharide), is a component of bacterial cell walls that we end up absorbing when we have suboptimal gut health. As a metabolic toxin, it then directly impairs our ability to produce energy, and is unsurprisingly is implicated in virtually all chronic health conditions (46, 47).
In fact, endotoxin is so effective at driving inflammation that it’s consistently used in research for just that purpose, and also happens to be the main factor driving sepsis, the leading cause of death in hospitalized patients and the 10th leading cause of death overall in the United States (48, 49, 50).
And that’s only one piece of gut health, without considering the importance of digesting and absorbing nutrients, the impact of other components of an unhealthy microbiome, and the direct inflammation and stress hormone production from an unhealthy gut, among other things.
The same can be said for inefficient glucose metabolism.
As we described earlier, inefficient glucose metabolism is the primary driver of insulin resistance and essentially leaves us with a lack of energy, excessive stress hormones, constant hunger, and a path toward degeneration.
But, when someone fasts and shifts to fat and ketone metabolism, they’re able to produce considerably energy with less stress than inefficient glucose metabolism, which can relieve many of these issues.
Now not only does the balance between gut relief, inefficient carbohydrate metabolism, and stress make sense physiologically, it’s also supported by the preliminary fasting research (as there isn’t much fasting research to date), where much of the benefits from fasting are mediated by gut relief (particularly from endotoxin) and the shift away from inefficient carb metabolism:
“An extended fasting period (i.e., gut rest) could also lead to reduced gut permeability and, as a result, to blunted postprandial endotoxemia (50, 61, 64, 73) and to blunted systemic inflammation (94, 102), which are typically elevated in obesity. Recently, investigators from the Salk Institute for Biological Studies reported that a brain–gut pathway activated in the brain during fasting acts to promote energy balance by enhancing gut epithelial integrity (95). Finally, jet-lag-induced dysbiosis in both mice and humans promotes glucose intolerance and obesity that are transferrable to germ-free mice upon fecal transplantation (101).” (51)
Not surprisingly, calorie restriction also tends to mimic this presentation for much the same reason, where the benefits of calorie restriction are mediated by changes in gut health that can then be replicated by a fecal transplant in animals that aren’t even under calorie restriction:
“… the microbiota alone is sufficient to enhance insulin sensitivity, improve tolerance to glucose and cold, and reduce fat content, and this effect is at least in part mediated by browning of the white fat depots… Together, these data suggest a molecular explanation of the microbiota-immune system-fat signaling axis, and imply the microbiota as a key player mediating the metabolic benefits of with large therapeutic potential.” (52)
Additionally, it was found that decreasing or preventing the response to endotoxin by TLR4 antagonism or knockout was enough to fully account for the benefits of calorie restriction, while artificially increasing endotoxin prevented the health benefits from calorie restriction:
“Consistent with the innate immunity-mediated CR-induced browning, the Tlr4 KO bone marrow-derived hematopoietic cells increase beige fat development in recipient mice irrespective of their genetic background, while Tlr4 KO mice are resistant to further improvements of their metabolic status during … Pharmacological treatment with a TLR4 antagonist phenocopied a number of -induced metabolic improvements and induced browning.” (52)
“Reconstituting LPS (Escherichia coli 055:B5) using osmotic minipumps at dose of 300 μg/kg/day was sufficient to completely revert the CR-mediated increase in the glucose tolerance without affecting the insulin levels during the test, and diminish the improved sensitivity to insulin and cold tolerance (Figures S4A–S4G). LPS replenishment in the CR mice completely prevented the CR-induced browning and the CR-induced increase in the M2 macrophage polarization and eosinophil infiltration (Figures S4H–S4J).” (52)
Considering the dramatic long-range effects of endotoxin, it’s no wonder that people experience a multitude of benefits from fasting, much like low-carb, ketogenic, or carnivore diets, or even simply caloric restriction.
But, the stress always catches up with us eventually…
Fasting in The Long-Term: The Cost of Stress
We’ve already discussed the stress trade-off – the short-term adaptation that allows us to handle immediate demands while incurring an energy debt that has to be repaid at some point – and this applies perfectly to fasting.
The deprivation of all nutrients, but particularly carbohydrates, through fasting is certainly stressful. And often fasting is paired with some variation of a low-carb diet, which only drives this stress further.
But the problem is that it doesn’t always feel this way at first. Instead, the stress hormones often make us feel really good initially, like the energy boost from a cup of coffee (without any cream or sugar of course).
Plus, the gut relief and shift away from inefficient glucose metabolism can also blunt the earlier effects of stress.
Yet over time, this stress debt accumulates and takes its toll in the form of slowing thyroid function, reproductive function, immune function, and on from there, leading to systemic degeneration.
Another major sign of this stress is muscle wasting, which has recently been demonstrated to occur during intermittent fasting (23). This finding was so impactful that the lead researcher, a cardiologist who had been fasting himself and recommending fasting to his patients for over 5 years, immediately stopped fasting (53).
Additionally, this recent study showed that fasting depleted vitamin D and raises estrogen. The researchers hypothesized that this was due to the body adjusting in anticipation of a longer term food shortage.
“We now show that the CYP2R1 enzyme may be repressed also functionally at the level of gene regulation. Twelve-hour fasting suppressed liver microsomal vitamin D 25-hydroxylation ∼50%, and after 24-h fasting, we were unable to detect any 25-OH-D formation. Thus, the first vitamin D bioactivation step is under the strict control of nutritional state. Although the acute food deprivation resulted in a strong effect on vitamin D 25-hydroxylase activity, this was not reflected in the plasma 25-OH-D concentration, presumably because of the long half-life of 25-OH-D (47). Therefore, it seems unlikely that short-term fasting would have a significant effect on vitamin D functions at the systemic level. This raises the question of the physiological purpose of the CYP2R1 repression during fasting. A likely explanation is that fasting launches physiological adjustment as precaution for possible longer-term food shortage“
Now what if you’re not pairing fasting with a low-carb diet, wouldn’t you be able to repay the energy debt?
Yes, if your environment is good enough the rest of the time you may be able to pay off the energy debt and more. But, considering the many insults we face on a daily basis (social and emotional stress, chemical exposure, poor food supply, etc.), adding to the debt is more likely than repaying it.
This is not to mention that, while being out of debt is great, the more “energy wealth” we accumulate, the further we move toward regeneration and improved health. So why would we ever want to incur a huge stress cost if we don’t have to?
And the good news is that we don’t! We can attain all the benefits of fasting without causing any of the stress.
A Side Note On Autophagy
I know some of you may still be wondering about autophagy, as many in favor of fasting will cite autophagy as one of its main benefits, if not its primary benefit.
(For those who aren’t aware, autophagy is a basic clean-up process in our cells that helps to clear away damaged components.)
The basic idea put forth here is that “damaged cellular components are bad, so cleaning up these damaged components is good, so doing things to increase autophagy is good.”
And while it’s true that cleaning up any damaged components is beneficial, that doesn’t mean we want to be doing things that increase autophagy.
Because the main thing that increases autophagy is stress and damage!
This is why anything that’s stressful or considered to be “hormetic” will increase autophagy – the autophagy is required to clean up the damage that’s caused.
This was explained clearly in this study:
“Autophagy is the major mechanism through which all cytoplasmic parts of post-mitotic cells can be renewed. Therefore, it is considered a vital cytoprotective process that prevents the accumulation of damaged cellular biomolecules and structures. This also applies to oxidative stress. If antioxidant enzyme systems and cellular antioxidants fail to prevent oxidative damage, autophagy takes effect as a second line protection response by degrading oxidatively damaged cellular structures. Accordingly oxidative stress and lipid peroxidation products have been shown to upregulate autophagy for prevention damage accumulation.”
In other words, exposing yourself to “hormetic” stressors to increase autophagy is like trying to solve a lack of clean-up by creating more of a mess!
Now, as proponents of fasting and hormesis like to point out, defects in autophagy are seen in various chronic health conditions.
And this makes sense – an inability for our cells to properly execute autophagy does signify a problem… an energy problem!
We know that these chronic health conditions are states of excess stress and a lack of energy.
And, a lack of energy will prevent proper cellular functioning in various ways, including preventing effective autophagy and other adaptive processes, as that same study supported:
“… autophagy is a highly energy consuming process which may be affected upon ATP deficit. The results obtained in our study suggest that already moderately reduced ATP levels may affect autophagy in RPE cells, thereby weakening this stress response.”
So in this case, adding on further stress and increasing the energy debt through “hormetic” stressors would only make the situation worse in the long run.
I discussed all this in more detail in these articles if you’re interested in a more in-depth explanation regarding the problems with hormesis and why focusing on stimulating autophagy, mitochondrial biogenesis, uncoupling, and other adaptive responses can lead us down a treacherous path.
Have Your Cake and Eat it Throughout The Day Too
Considering that the benefits of fasting result from relief from both poor gut health and inefficient glucose metabolism, the best approach would be to achieve the same benefits without the stress by improving gut health and glucose metabolism.
And the great news is that this not only is this entirely possible, it involves eating carbohydrates and having them consistently throughout the day.
But, it’s not quite that simple.
When it comes to gut health, here are a few good places to start:
1. Remove irritating foods
It helps to begin by removing the things that are irritating your gut, as Carnivore Aurelius has previously pointed out. Often this comes in the form of removing whole grains, legumes, nuts and seeds, and raw vegetables.
The tough-to-digest fibers and antinutrients in these foods inhibit our ability to digest our food and absorb nutrients, drive bacterial growth and endotoxin production, and also damage our gut barrier causing it to become permeable or “leaky” (54, 55, 56, 57, 58).
2. Favor saturated fats over the polyunsaturated fats (PUFA)
Taking in high-quality saturated fats will help to keep your small intestine clear of harmful microbes, both due to their own antimicrobial and endotoxin-protecting properties and their capacity to stimulate bile production, which also acts as an effective antimicrobial and detoxifier of endotoxin (59, 60, 61, 62, 63, 64, 65).
PUFA, on the other hand, will increase the inflammatory response to endotoxin while also inhibiting our ability to produce energy (which especially comes into play when it comes to glucose metabolism) (61, 66).
3. Favor fruits and roots
Fruits and roots are ideal carbohydrate sources, not only due to their lack of antinutrients, but also because of their polyphenol and bioflavonoid content, which have selective antimicrobial effects that help to rebalance our microbiome (
Just make sure the fruits are ripe and the roots are cooked well!
Not coincidentally, all of these things will help tremendously to improve glucose metabolism.
Because one of the main inhibitors of glucose metabolism is endotoxin and other gut toxins!
So, by improving our gut health we’ll also directly improve our ability to metabolize carbohydrates.
And, each of these steps also helps to improve our glucose metabolism through other means.
1. Remove irritating foods
The antinutrients in irritating foods primarily inhibit glucose metabolism in two ways (beyond contributing to endotoxin production and passage through the intestinal barrier).
First is that they bind with minerals like calcium, magnesium, zinc, copper, iron, and potassium, which inhibits their absorption and usage (76, 77, 78). And, all of these minerals play a vital role in energy production.
Second is that certain antinutrients, specifically saponins, function as goitrogens, meaning that they directly inhibit our thyroid function which is the major regular of our metabolism (79).
2. Favor saturated fats over the polyunsaturated fats (PUFA)
PUFA are another primary inhibitor of glucose metabolism as they directly decrease the efficiency of mitochondrial respiration when used as structural components in the mitochondria, convert to metabolites that inhibit mitochondrial respiration, and become damaged, which drives oxidative stress and further inhibits mitochondrial respiration (80, 81).
3. Favor fruits and roots
The stress hormones are one of the main inhibitors of efficient glucose metabolism, and eating adequate carbohydrates is the best way to keep the stress hormones low by supplying glucose for our blood sugar (82, 83). Furthermore, these carbohydrate sources, in addition to nutrient-dense protein sources like organ meats and seafood, supply the vitamins and minerals needed for efficient glucose metabolism.
It’s also worth mentioning that, considering that various organ systems (especially our brains) are constantly using sugar, a consistent supply of carbohydrates is necessary throughout the day to minimize the stress hormones. Having a carbohydrate-containing meal or snack every 3-4 hours is typically adequate to minimize the stress hormones and maximize glucose metabolism.
Improving gut health and glucose metabolism can certainly extend beyond these few steps, where microbial imbalances may need to be treated directly with targeted antimicrobials, various vitamin and mineral deficiencies may need to be addressed with nutrition or supplement strategies, and other aspects of lifestyle may also have to be adjusted to minimize stress.
But, in addition to stopping fasting, these are the most important steps to start and can make a huge difference in these crucial areas of health.
Feel free to check out The Energy Balance Podcast, follow me on social media (@jfwellness or Jay Feldman Wellness), and check out my website (www.jayfeldmanwellness.com) for more tips on improving gut health, minimizing stress, and maximizing your metabolism.
The information and articles (“the Content”) provided on the Carnivore Aurelius website are intended only as general health and wellness advice, and is for educational purposes only. The Content should not be construed as medical advice or information on diagnosing, treating, preventing, or mitigating disease. Always consult a healthcare professional before starting a new diet, exercise, ﬁtness plan, or health plan or program. You are encouraged to conﬁrm the Content obtained from this website with other sources, and review all information regarding any medical condition or the treatment of such condition with your healthcare provider. If you have questions regarding medical conditions or develop a health condition or disease, please consult with your healthcare provider. NEVER DISREGARD PROFESSIONAL MEDICAL ADVICE, DELAY SEEKING MEDICAL ADVICE OR TREATMENT, OR STOP CURRENT MEDICAL TREATMENT BECAUSE OF SOMETHING YOU HAVE READ ON THIS WEBSITE.
Weekly Motivational and Health Content
- Clarke DD, Sokoloff L. “Regulation of Cerebral Metabolic Rate.” In: Siegel GJ, Agranoff BW, Albers RW, et al., editors. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition. Philadelphia: Lippincott-Raven; 1999. Available from: https://www.ncbi.nlm.nih.gov/books/NBK28194/
- Mitrakou, A., et al. “Hierarchy of Glycemic Thresholds for Counterregulatory Hormone Secretion, Symptoms, and Cerebral Dysfunction.” The American journal of physiology, vol. 260, 1 Pt 1, 1991, E67-74. doi:10.1152/ajpendo.1991.260.1.E67.
- McEwen, Bruce S. “Protection and Damage from Acute and Chronic Stress: Allostasis and Allostatic Overload and Relevance to the Pathophysiology of Psychiatric Disorders.” Annals of the New York Academy of Sciences, vol. 1032, 2004, pp. 1–7. doi:10.1196/annals.1314.001.
- Chrousos, G. P. “The Role of Stress and the Hypothalamic-Pituitary-Adrenal Axis in the Pathogenesis of the Metabolic Syndrome: Neuro-Endocrine and Target Tissue-Related Causes.” International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity, 24 Suppl 2, 2000, S50-5. doi:10.1038/sj.ijo.0801278.
- Walker, B. R. “Cortisol–Cause and Cure for Metabolic Syndrome?” Diabetic medicine : a journal of the British Diabetic Association, vol. 23, no. 12, 2006, pp. 1281–88. doi:10.1111/j.1464-5491.2006.01998.x.
- Andrews, Robert C., et al. “Abnormal Cortisol Metabolism and Tissue Sensitivity to Cortisol in Patients with Glucose Intolerance.” The Journal of clinical endocrinology and metabolism, vol. 87, no. 12, 2002, pp. 5587–93. doi:10.1210/jc.2002-020048.
- Chiodini, Iacopo, et al. “Cortisol Secretion in Patients with Type 2 Diabetes: Relationship with Chronic Complications.” Diabetes care, vol. 30, no. 1, 2007, pp. 83–88. doi:10.2337/dc06-1267.
- Buttgereit, Frank, et al. “Bioenergetics of Immune Functions: Fundamental and Therapeutic Aspects.” Immunology today, vol. 21, no. 4, 2000, pp. 194–99. doi:10.1016/s0167-5699(00)01593-0.
- Björntorp, Per. “Body Fat Distribution, Insulin Resistance, and Metabolic Diseases.” Nutrition, vol. 13, no. 9, 1997, pp. 795–803. doi:10.1016/S0899-9007(97)00191-3.
- Wolkowitz, O. M., et al. “Stress Hormone-Related Psychopathology: Pathophysiological and Treatment Implications.” The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry, vol. 2, no. 3, 2001, pp. 115–43. doi:10.3109/15622970109026799.
- Mawdsley, J. E., and D. S. Rampton. “Psychological Stress in IBD: New Insights into Pathogenic and Therapeutic Implications.” Gut, vol. 54, no. 10, 2005, pp. 1481–91. doi:10.1136/gut.2005.064261.
- Cushman, P. “Glucocorticoids and the Gastrointestinal Tract: Current Status.” Gut, vol. 11, no. 6, 1970, pp. 534–39. doi:10.1136/gut.11.6.534.
- DeGroot LJ. “The Non-Thyroidal Illness Syndrome.” Updated 2015 Feb 1. In Endotext: De Groot LJ, Chrousos G, Dungan K, et al., editors. Endotext . South Dartmouth (MA): MDText.com, Inc. Available from: https://www.ncbi.nlm.nih.gov/books/NBK285570/.
- Chopra, I. J., et al. “Opposite Effects of Dexamethasone on Serum Concentrations of 3,3′,5′-Triiodothyronine (Reverse T3) and 3,3’5-Triiodothyronine (T3).” The Journal of clinical endocrinology and metabolism, vol. 41, no. 5, 1975, pp. 911–20. doi:10.1210/jcem-41-5-911.
- Bianco, A. C., et al. “The Role of Glucocorticoids in the Stress-Induced Reduction of Extrathyroidal 3,5,3′-Triiodothyronine Generation in Rats.” Endocrinology, vol. 120, no. 3, 1987, pp. 1033–38. doi:10.1210/endo-120-3-1033.
- Brtko, Július, et al. “Stress Is Associated with Inhibition of Type I Iodothyronine 5′-Deiodinase Activity in Rat Liver.” Annals of the New York Academy of Sciences, vol. 1018, 2004, pp. 219–23. doi:10.1196/annals.1296.026.
- Cavalieri, R. R., et al. “Effects of Dexamethasone on Kinetics and Distribution of Triiodothyronine in the Rat.” Endocrinology, vol. 114, no. 1, 1984, pp. 215–21. doi:10.1210/endo-114-1-215.
- Langer, P. “.” . Bratislavske lekarske listy, vol. 90, no. 7, 1989, pp. 520–31.
- Alemany, Marià. “Do the Interactions Between Glucocorticoids and Sex Hormones Regulate the Development of the Metabolic Syndrome?” Frontiers in endocrinology, vol. 3, 2012, p. 27. doi:10.3389/fendo.2012.00027.
- Boelen, Anita, et al. “Fasting-Induced Changes in the Hypothalamus-Pituitary-Thyroid Axis.” Thyroid : official journal of the American Thyroid Association, vol. 18, no. 2, 2008, pp. 123–29. doi:10.1089/thy.2007.0253.
- Bergendahl, M., et al. “Fasting as a Metabolic Stress Paradigm Selectively Amplifies Cortisol Secretory Burst Mass and Delays the Time of Maximal Nyctohemeral Cortisol Concentrations in Healthy Men.” The Journal of clinical endocrinology and metabolism, vol. 81, no. 2, 1996, pp. 692–99. doi:10.1210/jcem.81.2.8636290.
- RIXON, R. H., and J. A. STEVENSON. “Factors Influencing Survival of Rats in Fasting; Metabolic Rate and Body Weight Loss.” The American journal of physiology, vol. 188, no. 2, 1957, pp. 332–36. doi:10.1152/ajplegacy.1922.214.171.1242.
- Lowe, Dylan A., et al. “Effects of Time-Restricted Eating on Weight Loss and Other Metabolic Parameters in Women and Men with Overweight and Obesity: The TREAT Randomized Clinical Trial.” JAMA internal medicine, vol. 180, no. 11, 2020, pp. 1491–99. doi:10.1001/jamainternmed.2020.4153.
- Bouché, Clara, et al. “The Cellular Fate of Glucose and Its Relevance in Type 2 Diabetes.” Endocrine reviews, vol. 25, no. 5, 2004, pp. 807–30. doi:10.1210/er.2003-0026.
- Del Prato, S., et al. “Characterization of Cellular Defects of Insulin Action in Type 2 (Non-Insulin-Dependent) Diabetes Mellitus.” The Journal of clinical investigation, vol. 91, no. 2, 1993, pp. 484–94. doi:10.1172/JCI116226.
- Simoneau, J. A., and D. E. Kelley. “Altered Glycolytic and Oxidative Capacities of Skeletal Muscle Contribute to Insulin Resistance in NIDDM.” Journal of applied physiology (Bethesda, Md. : 1985), vol. 83, no. 1, 1997, pp. 166–71. doi:10.1152/jappl.19126.96.36.199.
- Petersen, Kitt Falk, et al. “Mitochondrial Dysfunction in the Elderly: Possible Role in Insulin Resistance.” Science (New York, N.Y.), vol. 300, no. 5622, 2003, pp. 1140–42. doi:10.1126/science.1082889.
- Sonksen, P., and J. Sonksen. “Insulin: Understanding Its Action in Health and Disease.” British journal of anaesthesia, vol. 85, no. 1, 2000, pp. 69–79. doi:10.1093/bja/85.1.69.
- Sonksen, P. H. “Insulin, Growth Hormone and Sport.” The Journal of endocrinology, vol. 170, no. 1, 2001, pp. 13–25. doi:10.1677/joe.0.1700013.
- Li, Xiao C., and Jia L. Zhuo. “Current Insights and New Perspectives on the Roles of Hyperglucagonemia in Non-Insulin-Dependent Type 2 Diabetes.” Current hypertension reports, vol. 15, no. 5, 2013, pp. 522–30. doi:10.1007/s11906-013-0383-y.
- Archer, Edward, et al. “Cell-Specific “Competition for Calories” Drives Asymmetric Nutrient-Energy Partitioning, Obesity, and Metabolic Diseases in Human and Non-Human Animals.” Frontiers in physiology, vol. 9, 2018, p. 1053. doi:10.3389/fphys.2018.01053.
- Fukagawa, N. K., et al. “High-Carbohydrate, High-Fiber Diets Increase Peripheral Insulin Sensitivity in Healthy Young and Old Adults.” The American journal of clinical nutrition, vol. 52, no. 3, 1990, pp. 524–28. doi:10.1093/ajcn/52.3.524.
- Kahleova, Hana, et al. “A Plant-Based High-Carbohydrate, Low-Fat Diet in Overweight Individuals in a 16-Week Randomized Clinical Trial: The Role of Carbohydrates.” Nutrients, vol. 10, no. 9, 2018, doi:10.3390/nu10091302.
- Chen, M., et al. “Insulin Resistance and Beta-Cell Dysfunction in Aging: The Importance of Dietary Carbohydrate.” The Journal of clinical endocrinology and metabolism, vol. 67, no. 5, 1988, pp. 951–57. doi:10.1210/jcem-67-5-951.
- Soop, M., et al. “Preoperative Oral Carbohydrate Treatment Attenuates Immediate Postoperative Insulin Resistance.” American journal of physiology. Endocrinology and metabolism, vol. 280, no. 4, 2001, E576-83. doi:10.1152/ajpendo.2001.280.4.E576.
- Pérez-Jiménez, F., et al. “A Mediterranean and a High-Carbohydrate Diet Improve Glucose Metabolism in Healthy Young Persons.” Diabetologia, vol. 44, no. 11, 2001, pp. 2038–43. doi:10.1007/s001250100009.
- Himsworth, H. P. “Dietetic Factors Influencing the Glucose Tolerance and the Activity of Insulin.” The Journal of physiology, vol. 81, no. 1, 1934, pp. 29–48. doi:10.1113/jphysiol.1934.sp003113.
- Bisschop, P. H., et al. “Dietary Fat Content Alters Insulin-Mediated Glucose Metabolism in Healthy Men.” The American journal of clinical nutrition, vol. 73, no. 3, 2001, pp. 554–59. doi:10.1093/ajcn/73.3.554.
- Kinzig, Kimberly P., et al. “Insulin Sensitivity and Glucose Tolerance Are Altered by Maintenance on a Ketogenic Diet.” Endocrinology, vol. 151, no. 7, 2010, pp. 3105–14. doi:10.1210/en.2010-0175.
- Hall, Kevin D., et al. “The Carbohydrate-Insulin Model of Obesity Is Difficult to Reconcile with Current Evidence.” JAMA internal medicine, vol. 178, no. 8, 2018, pp. 1103–05. doi:10.1001/jamainternmed.2018.2920.
- Hall, K. D. “A Review of the Carbohydrate-Insulin Model of Obesity.” European journal of clinical nutrition, vol. 71, no. 3, 2017, pp. 323–26. doi:10.1038/ejcn.2016.260.
- Hall, Kevin D., et al. “Calorie for Calorie, Dietary Fat Restriction Results in More Body Fat Loss Than Carbohydrate Restriction in People with Obesity.” Cell metabolism, vol. 22, no. 3, 2015, pp. 427–36. doi:10.1016/j.cmet.2015.07.021.
- Hall, Kevin D., et al. “Energy Expenditure and Body Composition Changes After an Isocaloric Ketogenic Diet in Overweight and Obese Men.” The American journal of clinical nutrition, vol. 104, no. 2, 2016, pp. 324–33. doi:10.3945/ajcn.116.133561.
- Axen, Kathleen V., and Kenneth Axen. “Very Low-Carbohydrate Versus Isocaloric High-Carbohydrate Diet in Dietary Obese Rats.” Obesity (Silver Spring, Md.), vol. 14, no. 8, 2006, pp. 1344–52. doi:10.1038/oby.2006.152.
- Team FPS. “Exercise Induced Stress.” Retrieved from: https://www.functionalps.com/blog/2012/03/01/exercise-induced-stress/
- Crouser, Elliott D., et al. “Endotoxin-Induced Mitochondrial Damage Correlates with Impaired Respiratory Activity.” Critical care medicine, vol. 30, no. 2, 2002, pp. 276–84. doi:10.1097/00003246-200202000-00002.
- Wei, Junping, et al. “Endotoxin-Stimulated Nitric Oxide Production Inhibits Expression of Cytochrome C Oxidase in ANA-1 Murine Macrophages.” Journal of immunology (Baltimore, Md. : 1950), vol. 168, no. 9, 2002, pp. 4721–27. doi:10.4049/jimmunol.168.9.4721.
- Opal, Steven M. “Endotoxins and Other Sepsis Triggers.” Contributions to nephrology, vol. 167, 2010, pp. 14–24. doi:10.1159/000315915.
- Deutschman, Clifford S., and Kevin J. Tracey. “Sepsis: Current Dogma and New Perspectives.” Immunity, vol. 40, no. 4, 2014, pp. 463–75. doi:10.1016/j.immuni.2014.04.001.
- Martin, Greg S., et al. “The Epidemiology of Sepsis in the United States from 1979 Through 2000.” The New England journal of medicine, vol. 348, no. 16, 2003, pp. 1546–54. doi:10.1056/NEJMoa022139.
- Patterson, Ruth E., and Dorothy D. Sears. “Metabolic Effects of Intermittent Fasting.” Annual review of nutrition, vol. 37, 2017, pp. 371–93. doi:10.1146/annurev-nutr-071816-064634.
- Fabbiano, Salvatore, et al. “Functional Gut Microbiota Remodeling Contributes to the Caloric Restriction-Induced Metabolic Improvements.” Cell metabolism, vol. 28, no. 6, 2018, 907-921.e7. doi:10.1016/j.cmet.2018.08.005.
- Gabby Landsverk. “A doctor who has been intermittent fasting for years said he quit because his new study showed it has little benefit for health or weight loss.” Retrieved from: https://www.insider.com/doctor-no-longer-supports-fasting-diet-study-found-few-benefits-2020-10
- Vasconcelos, Ilka M., and José Tadeu A. Oliveira. “Antinutritional Properties of Plant Lectins.” Toxicon : official journal of the International Society on Toxinology, vol. 44, no. 4, 2004, pp. 385–403. doi:10.1016/j.toxicon.2004.05.005.
- Banwell, J. G., et al. “Bacterial Overgrowth by Indigenous Microflora in the Phytohemagglutinin-Fed Rat.” Canadian journal of microbiology, vol. 34, no. 8, 1988, pp. 1009–13. doi:10.1139/m88-177.
- Punder, Karin de, and Leo Pruimboom. “The Dietary Intake of Wheat and Other Cereal Grains and Their Role in Inflammation.” Nutrients, vol. 5, no. 3, 2013, pp. 771–87. doi:10.3390/nu5030771.
- Sjölander, A., et al. “The Effect of Concanavalin a and Wheat Germ Agglutinin on the Ultrastructure and Permeability of Rat Intestine. A Possible Model for an Intestinal Allergic Reaction.” International archives of allergy and applied immunology, vol. 75, no. 3, 1984, pp. 230–36. doi:10.1159/000233621.
- Greer, F., and A. Pusztai. “Toxicity of Kidney Bean (Phaseolus Vulgaris) in Rats: Changes in Intestinal Permeability.” Digestion, vol. 32, no. 1, 1985, pp. 42–46. doi:10.1159/000199215.
- Kabara, John J. “Antimicrobial Agents Derived from Fatty Acids.” Journal of the American Oil Chemists’ Society, vol. 61, no. 2, 1984, pp. 397–403. doi:10.1007/BF02678802.
- Porter, Edith. “Antimicrobial Lipids: Emerging Effector Molecules of Innate Host Defense.” World Journal of Immunology, vol. 5, no. 2, 2015, p. 51. doi:10.5411/wji.v5.i2.51.
- Nanji, A. A., et al. “Dietary Saturated Fatty Acids down-Regulate Cyclooxygenase-2 and Tumor Necrosis Factor Alfa and Reverse Fibrosis in Alcohol-Induced Liver Disease in the Rat.” Hepatology (Baltimore, Md.), vol. 26, no. 6, 1997, pp. 1538–45. doi:10.1002/hep.510260622.
- Begley, Máire, et al. “The Interaction Between Bacteria and Bile.” FEMS microbiology reviews, vol. 29, no. 4, 2005, pp. 625–51. doi:10.1016/j.femsre.2004.09.003.
- Ridlon, Jason M., et al. “Bile Acids and the Gut Microbiome.” Current opinion in gastroenterology, vol. 30, no. 3, 2014, pp. 332–38. doi:10.1097/MOG.0000000000000057.
- Nie, Yang-fan, et al. “Cross-Talk Between Bile Acids and Intestinal Microbiota in Host Metabolism and Health.” Journal of Zhejiang University. Science. B, vol. 16, no. 6, 2015, pp. 436–46. doi:10.1631/jzus.B1400327.
- Bertók, Lóránd. “Bile Acids in Physico-Chemical Host Defence.” Pathophysiology : the official journal of the International Society for Pathophysiology, vol. 11, no. 3, 2004, pp. 139–45. doi:10.1016/j.pathophys.2004.09.002.
- Kirpich, Irina A., et al. “The Type of Dietary Fat Modulates Intestinal Tight Junction Integrity, Gut Permeability, and Hepatic Toll-Like Receptor Expression in a Mouse Model of Alcoholic Liver Disease.” Alcoholism, clinical and experimental research, vol. 36, no. 5, 2012, pp. 835–46. doi:10.1111/j.1530-0277.2011.01673.x.
- Górniak, Ireneusz, et al. “Comprehensive Review of Antimicrobial Activities of Plant Flavonoids.” Phytochemistry Reviews, vol. 18, no. 1, 2019, pp. 241–72. doi:10.1007/s11101-018-9591-z.
- Coppo, Erika, and Anna Marchese. “Antibacterial Activity of Polyphenols.” Current pharmaceutical biotechnology, vol. 15, no. 4, 2014, pp. 380–90. doi:10.2174/138920101504140825121142.
- Rastmanesh, Reza. “High Polyphenol, Low Probiotic Diet for Weight Loss Because of Intestinal Microbiota Interaction.” Chemico-biological interactions, vol. 189, 1-2, 2011, pp. 1–8. doi:10.1016/j.cbi.2010.10.002.
- Kawabata, Kyuichi, et al. “Role of Intestinal Microbiota in the Bioavailability and Physiological Functions of Dietary Polyphenols.” Molecules (Basel, Switzerland), vol. 24, no. 2, 2019, doi:10.3390/molecules24020370.
- Edwards, C. A., et al. “Polyphenols and Health: Interactions Between Fibre, Plant Polyphenols and the Gut Microbiota.” Nutrition bulletin, vol. 42, no. 4, 2017, pp. 356–60. doi:10.1111/nbu.12296.
- Ozdal, Tugba, et al. “The Reciprocal Interactions Between Polyphenols and Gut Microbiota and Effects on Bioaccessibility.” Nutrients, vol. 8, no. 2, 2016, p. 78. doi:10.3390/nu8020078.
- Huang, Chung-Yen, et al. “Glucose-Mediated Cytoprotection in the Gut Epithelium Under Ischemic and Hypoxic Stress.” Histology and histopathology, vol. 32, no. 6, 2017, pp. 543–50. doi:10.14670/HH-11-839.
- Babic, I., et al. “Antimicrobial Activity of Shredded Carrot Extracts on Food-Borne Bacteria and Yeast.” The Journal of applied bacteriology, vol. 76, no. 2, 1994, pp. 135–41. doi:10.1111/j.1365-2672.1994.tb01608.x.
- Engevik, Melinda A., et al. “Prebiotic Properties of Galursan HF 7K on Mouse Gut Microbiota.” Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, vol. 32, no. 7, 2013, pp. 96–110. doi:10.1159/000356631.
- K O Soetan, and O E Oyewole. The Need for Adequate Processing to Reduce the Anti- Nutritional Factors in Plants Used as Human Foods and Animal Feeds: A Review. 2009 3, www.researchgate.net/publication/266884320_The_need_for_adequate_processing_to_reduce_the_anti-_nutritional_factors_in_plants_used_as_human_foods_and_animal_feeds_A_review.
- Nävert, B., et al. “Reduction of the Phytate Content of Bran by Leavening in Bread and Its Effect on Zinc Absorption in Man.” The British journal of nutrition, vol. 53, no. 1, 1985, pp. 47–53. doi:10.1079/bjn19850009.
- Bohn, Torsten, et al. “Phytic Acid Added to White-Wheat Bread Inhibits Fractional Apparent Magnesium Absorption in Humans.” The American journal of clinical nutrition, vol. 79, no. 3, 2004, pp. 418–23. doi:10.1093/ajcn/79.3.418.
- Kimura, S., et al. “Development of Malignant Goiter by Defatted Soybean with Iodine-Free Diet in Rats.” Gan, vol. 67, no. 5, 1976, pp. 763–65.
- Jay Feldman. “Fats: We’ve Got It All Wrong.” Retrieved from: https://jayfeldmanwellness.com/fats-weve-got-it-all-wrong/
- Jay Feldman. “Omega-3s Are Not The “Healthy Fats.” Retrieved from: https://jayfeldmanwellness.com/omega-3s-are-not-the-healthy-fats/
- Laugero, Kevin D. “Reinterpretation of Basal Glucocorticoid Feedback: Implications to Behavioral and Metabolic Disease.” Vitamins and Hormones: Advances in Research and Applications, edited by Gerald Litwack, vol. 69, Elsevier/Academic Press, 2004, pp. 1–29. Vitamins and Hormones V. 69.
- Dhar, H. L., et al. “The Relationship of the Blood Sugar Level to the Severity of Anaphylactic Shock.” British Journal of Pharmacology and Chemotherapy, vol. 31, no. 2, 1967, pp. 351–55. doi:10.1111/j.1476-5381.1967.tb02005.x.