GLP-1 Receptor Agonists and Vitamin C: A Powerful Anti-Aging Combination

10/31/2025 by Dr. Thomas Levy

Editorial Introduction
By Richard Z. Cheng, M.D., Ph.D.
Editor-in-Chief, Orthomolecular Medicine News Service

When Dr. Thomas E. Levy sent me his manuscript, "GLP-1 Receptor Agonists and Vitamin C: A Powerful Anti-Aging Combination," he remarked that it might be the most important paper he has ever written. I agree-it is a bold, elegantly reasoned exploration of how vitamin C, redox biology, and modern metabolic therapies intersect at the frontier of preventive and restorative medicine.

Dr. Levy's work reminds us that the essence of health lies not in isolated molecules or single pathways, but in the redox equilibrium of the whole organism. By proposing that GLP-1 receptor agonists (the class of drugs now revolutionizing obesity and diabetes care) exert many of their effects through enhanced intracellular vitamin C uptake and redox normalization, he bridges two worlds often seen as separate: pharmacologic endocrinology and nutritional biochemistry. His central insight-that oxidative stress and vitamin C deficiency define the terrain of disease-aligns profoundly with the principles of Orthomolecular Medicine first articulated by Linus Pauling and Abram Hoffer.

At the same time, the article opens a valuable dialogue within our broader Integrative Orthomolecular Medicine (IOM) framework. From the IOM perspective, GLP-1 receptor agonists may be viewed not as endpoints, but as proof-of-concept pharmacologic tools that demonstrate how restoring metabolic and redox homeostasis reverses disease. The same physiologic benefits-improved insulin sensitivity, appetite regulation, and mitochondrial efficiency-can often be achieved through non-drug means:

  • Dietary optimization (low-carbohydrate, minimally processed foods)
  • Micronutrient repletion (vitamin C, magnesium, zinc, selenium, omega-3s)
  • Detoxification and physical activity, both of which lower oxidative burden and naturally enhance GLP-1 signaling.

Obesity, diabetes, and metabolic aging are multifactorial conditions driven by toxic exposures, nutrient deficits, and lifestyle imbalances. GLP-1 agonists demonstrate that metabolic flexibility can be pharmacologically restored-but orthomolecular and lifestyle interventions show it can also be restored naturally and sustainably.

In this sense, Dr. Levy's article does more than discuss a class of drugs. It redefines the conversation about aging and chronic disease: from one of symptom suppression to one of metabolic restoration. His biochemical reasoning is meticulous, and his conceptual leap-from redox biology to clinical practice-is visionary.

I encourage readers to approach this paper as both a scientific treatise and a philosophical challenge. It invites us to look beyond categories-drug vs. nutrient, mechanism vs. cause-and toward a unified model of health centered on cellular redox renewal. This is precisely the integrative vision that the Orthomolecular Medicine movement has long championed.

The following article is published in full, without editorial modification, in recognition of Dr. Levy's original voice and contribution to the field.

Overview

Nearly everyone today is aware of the highly effective weight loss drugs literally sweeping the planet. This weight loss is consistently and reliably induced by a group of drugs that imitate the actions of glucagon-like peptide-1 (GLP-1) by binding its natural receptor sites. Known as GLP-1 receptor agonists (GLP-1RAs), they produce the same physiological response as GLP-1, but for an extended period, as natural GLP-1 only has a plasma half-life of 2 or 3 minutes before being degraded by an enzyme known as dipeptidyl peptidase (DPP4). The GLP-1RAs can have half-lives from hours to days depending on type, dose, and method of administration, resulting in a substantial prolongation of the physiological effects of GLP-1.

GLP-1 is a 30-amino acid hormone secreted by cells in the ileum, the colon, the pancreatic α cells, and the central nervous system. [1,2] This hormone, as well as the GLP-1 receptor agonists:

  • Promote insulin release by binding GLP-1 receptors in the pancreatic β cells
  • Stimulate the proliferation and differentiation of those β cells while inhibiting their demise (apoptosis)
  • Reduce the secretion of glucagon (an agent that releases new glucose from its storage in liver glycogen) from the pancreatic α cells, helping to decrease circulating blood glucose levels
  • Delay gastric emptying
  • Reduce appetite
  • Increase sense of fullness in the stomach (satiety)

All these effects work to better control blood glucose levels and facilitate weight loss, including in patients without diabetes. [3,4]

Because of these glucose-modulating properties, GLP-1 receptor agonists have been used for the treatment of type 2 diabetes mellitus, first receiving official approval for this treatment application in 2005. [5] However, GLP-1 receptors that can be bound and activated are not only present in the pancreas, but also in many other tissues throughout the body, accounting for a wide variety of physiological and clinical effects, beyond just improved glycemic control. [6,7]

Vitamin C (VC) and the Immune System

Increased oxidative stress is primarily due to increased intracellular biomolecule oxidation, although it also can exist in the extracellular spaces. There is no disease "state" beyond that of the presence, degree, type, and distribution of the biomolecules that have been oxidized (electron-depleted). The resulting disease expression comes from the fact that oxidized biomolecules no longer function and contribute to normal metabolism. Such excessive oxidation only comes from toxins, which take and keep the electrons they steal, depleting the size of the electron pool in the body. [8] A molecule cannot be toxic unless it oxidizes biomolecules.

The intracellular vitamin C (VC) level is the marker indicating whether a cell is healthy or diseased. When a diseased cell regains a normal cytoplasmic level of VC, it once again becomes completely healthy. While many different factors work together in restoring intracellular VC levels to normal, that must still be the ultimate goal of any successful treatment protocol for any medical condition. If it can be achieved throughout the tissues and organs of the body, optimal health will always be realized.

VC has a unique relationship with the immune system. The immune system only works to quench inflammation wherever it occurs in the body. However, inflammation only occurs in cells and tissues where VC is severely depleted to completely absent. When the VC levels in inflamed tissues are restored to normal, inflammation is completely resolved. A state of advanced VC deficiency is the SAME as a state of advanced inflammation. Either state cannot exist in the absence of the other.

Acute inflammation is the sole trigger of an acute immune response. Such an acute immune response is initiated by the influx of monocytes, cells containing 80-fold (8,000%) or more VC than is in the blood. [9] As the VC content in the inflamed tissue rises, the degree of inflammation correspondingly declines. Also, areas of acute inflammation frequently involve either overt infection or a low-grade pathogen colonization. Pathogens are the most common sources of new toxins (pro-oxidants) in the body. Other immune cells, which contain lesser but still very large amounts of VC, follow the monocytes into the inflamed tissue in order to engulf, kill, and metabolize pathogens which further work to increase the levels of VC in the affected tissue. Along with the VC, monocytes also contain substantial amounts of magnesium and hydrogen peroxide. This trio of components is ideally suited to resolving infections while increasing antioxidant status in those cells. Once the pro-oxidant pathogens are gone, the VC present in the monocytes can more easily restore a normal oxidative status. What all of this means, then, is:

The sole purpose of the immune system is to restore VC levels to normal wherever they are deficient.

Immunology textbooks are filled with countless metabolic pathways promoted and inhibited by numerous agents, and with a mind-numbing array of abbreviations. However, the elegant simplicity of the assertion above should always be kept in mind. When there is no VC-deficient inflamed tissue to be addressed, the immune system is largely clinically inactive and basically in a standby mode, waiting to respond to the appearance of new pathogens and/or toxins in previously normal tissue.

Vitamin C and Cortisol: A Unique Relationship

Cortisol is the natural hormone released by the adrenal glands in large amounts when the blood receives a significant acute surge of oxidative stress, as with a new infection or a new toxin exposure. This is commonly referred to as the stress-induced "fight-or-flight" response. What happens in most animals, but very few humans, is the accelerated conversion of glucose to VC via a four-enzyme sequence in the liver. However, most humans have an epigenetic defect in the translation and expression of the fourth enzyme, L-gulonolactone oxidase (GULO), and the conversion of glucose to VC does not take place.

As it turns out, cortisol is not really an anti-inflammatory agent itself, but only one of the primary ways in which increased amounts of VC are ushered from the extracellular space into the cytoplasm of the cells. [10,11] As explained above, VC is the only real anti-inflammatory agent, as the anti-inflammatory property ascribed to cortisol is simply due to its ability to increase VC uptake into the cells, reducing the numbers of oxidized biomolecules contributing to any disease expression. Other antioxidants can quell inflammation to a lesser degree, but the antioxidant power of VC reigns supreme as the primary anti-inflammatory agent in all the cells (and tissues and organs) in the body.

Cortisol (and the synthetic corticosteroids) not only work with VC as described above, but they can also readily do more harm than good when VC is not being synthesized from glucose stores to interact with them in the blood (as is the case with most humans). When the VC synthesis is occurring the glucose stores are being consumed. However, when the fourth enzyme (GULO) is absent, the glucose not only accumulates, but the increased cortisol surge also results in the formation of new glucose via a process known as gluconeogenesis. The adrenal glands do not "know" VC is not being synthesized, and the gluconeogenesis occurs to make sure the glucose substrate for making new VC does not get used up, as would occur when the liver has a normal presence of GULO. But when VC is not being made, the new glucose simply adds to the unconverted glucose to elevate glucose levels and keep them high. This is why long-term corticosteroid usage often results in compromised glucose metabolism and even frank diabetes mellitus. Furthermore, gluconeogenesis uses up muscle protein to make the new glucose, accounting for the muscle wasting seen in long-term steroid administration in the absence of sufficient VC supplementation. [12]

For many obese individuals, the excess accumulation of fat is mostly due to the inability to properly compensate for the epigenetic defect preventing the body from converting glucose into vitamin C. While overeating is a problem, it cannot simply be concluded as being the only important reason for being overweight.

Hydroxytyrosol supplementation has been shown to increase endogenous VC levels. It appears that olive leaf extract with a high enough concentration of hydroxytyrosol can significantly lessen the impact of the epigenetic defect described above. [13]

When VC intake is minimal, the adrenal glands respond with a chronically increased release of cortisol in order to attempt to compensate for the decreased intracellular levels of VC. In fact, many cases of hypercortisolemia (increased cortisol blood levels) are secondary to the adrenal response to depleted levels of VC inside the cells, along with the lack of available extracellular VC for cortisol to push into the cells. Female patients diagnosed with functional hypercortisolemia due to unspecific chronic stress dropped their cortisol levels significantly after VC supplementation. Only 1,000 mg of VC daily was administered. Larger multi-gram VC doses may well completely resolve this chronic excess release of cortisol. [14] Similar drops in the elevated cortisol levels were seen in ultramarathon runners taking VC, supplementing either 1,000 mg or 1,500 mg daily. [15,16] The chronic supplementation of multigram doses of VC should completely resolve most cases of hypercortisolemia.

Vitamin C and Insulin

Another agent that works to directly usher VC into cells is insulin. Since only relatively minor enzymatic modifications in the liver can turn glucose into VC as noted above, VC and glucose are very similar molecules. As such, when either a large glucose load or a large VC load is introduced into the blood, the pancreas responds with a large release of insulin, as it cannot differentiate between the two substances. The increased cell wall transporters formed by the action of insulin inside the cells also cannot differentiate between the two substances, and glucose and VC compete directly with each other in entering the cells through these transporters that have been primed by insulin. [17] As a result, in uncontrolled diabetes with chronically high glucose levels, intracellular VC levels can never be achieved and are always severely depleted. This "intracellular scurvy" is the major factor that results in uncontrolled diabetes being such a clinically devastating disease.

Insulin has been documented to be a major healing factor. There is likely no agent more powerful in this regard than insulin. Furthermore, the entire reason for this powerful healing impact is that insulin directly and substantially promotes the uptake of the most important healing factor in the body, vitamin C, into the cells. Reversal of excess biomolecule oxidation IS healing, and increased intracellular VC levels must be achieved for this to occur. Much research, including large, prospective, placebo-controlled, and double-blinded studies, have documented this striking healing impact of insulin, whether applied systemically in the body or locally on a wound site, and either in diabetic or non-diabetic subjects. [18-28] When insulin and VC are in the blood in substantial amounts, especially in the setting of decreased glucose availability, healing is both rapid and of optimal quality. Vitamin C is the essential and primary factor for healing. [29] And in spite of all this research, few (if any?) wound centers around the world utilize applications of insulin with vitamin C to assure rapid and quality healing.

Vitamin C and Adipose Tissue

As with all other conditions in the body, the pathophysiology of obesity relates directly to chronically increased oxidative stress and the reaction of the body to its presence. Adipocytes (fat cells) increase in both number and size as more oxidative stress is encountered. [30] When sufficient VC is not present as well, the pro-oxidants or toxins comprising the increased oxidative stress go unneutralized. When they go unneutralized, the body seeks to counter their toxic impact by a compensatory mechanism. This mechanism, quite simply, is the production of more fat to put those toxins in storage and render them unavailable to most biomolecules, making them relatively nontoxic. In other words, chronically low plasma levels of vitamin C result in the formation of more fat to "buffer" the toxins that are not being neutralized by sufficient vitamin C on an ongoing basis. A chronically low plasma VC level is a major factor in causing and sustaining weight gain and obesity.

Multiple weight-related parameters, including body mass index, waist circumference, and body fat quantity, are inversely related to plasma vitamin C levels, as well as to measures of total antioxidant capacity. [31-33] Significantly lower levels of vitamin C, along with vitamins E, D, and B1, were seen in morbidly obese subjects relative to healthy controls. [34] Low magnesium levels, another major factor in causing and sustaining oxidative stress, was also seen in obese individuals. [35] The steady state of fat cell metabolism in obesity works to maintain low-grade inflammation, with fatty tissue releasing many different inflammatory mediators. [36]

In an animal study VC supplementation was able to reduce the weight gain that would otherwise be expected in a high fat diet designed to cause weight gain. [37] VC supplementation has also been shown to induce weight loss in guinea pigs (an animal with the same inability to make VC in the liver as the human). [38] In severely obese patients, a double-blind placebo-controlled administration of 3,000 mg of VC daily vs. placebo resulted in a clear-cut loss of weight in the treated group. [39] Multiple studies have documented the ability of VC to play an important role in both the treatment and prevention of obesity. [40,41] By itself, weight reduction can significantly improve antioxidant enzyme status in the body, which would be expected from a decreased need for toxins to be stored. [42] The primary conclusion of all these studies is that taking enough vitamin C neutralizes circulating toxins before they can stimulate new fat cell formation and be stored in those cells, resulting in weight gain. Conversely, keeping VC intake relatively low works to stimulate fat formation to deal with the circulating toxins that the VC deficiency is incapable of addressing and neutralizing.

Clinical Impact of GLP-1 Receptor Agonists (GLP-RAs)

There is a substantial variety of GLP-1 receptor agonist drugs (GLP-1RAs) available today. They all have similar physiological effects. Dose, frequency of dosing, half-life, and oral vs subcutaneous injection are the primary factors that determine the differences among them. As with literally any other drug or therapeutic agent, significant negative side effects can eventually be realized when an agent is taken in a high enough dose and when rapidly escalated in amount. [43] Low-dose and oral administrations are virtually devoid of substantial side effects. And even the more highly dosed and injectable applications that can cause clear side effects will dissipate in the degree of this effect over time. Overall, these are highly effective drugs with a minimal side effect profile, and they are very safe when taken correctly, even in patients with significant medical conditions. [44,45]

As many tissues and organs have GLP-1 receptor sites, many physiological effects beyond improved glucose metabolism and weight loss have been documented. These GLP-1 receptor site locations include the following:

  • Central nervous system, including the hypothalamus, brainstem, and other sites that are involved in appetite regulation and energy homeostasis. [46] Also receptor sites working to promote olfactory function and to prevent neurological complications, cognitive impairment, and peripheral neuropathy. [47,48] Also promotion of stem cells and progenitor cells in the brain. [49]
  • Gastrointestinal tract, playing a role in gut motility and hormone secretion
  • Heart and blood vessels
  • Kidneys [50]

Aside from the GLP-1RAs effects on glucose and weight loss, many very positive clinical effects have been observed and documented.

Most importantly, GLP-1RA drugs have been consistently shown to decrease all-cause mortality, which is the ultimate research parameter to determine the true value of a nutrient or drug, and whether minor side effects present long-term health concerns. [51-55]

Other documented and significant positive clinical and laboratory effects of GLP-1RAs include the following:

  • General anti-inflammatory impact [56]
  • Decreased C-reactive protein (CRP) levels [57]
  • Lessens development of periodontitis, with documentation that VC-containing monocytes accumulate in the inflamed cells [58]
  • Marked renal protection in chronic kidney disease [59]
  • Reduced cardiovascular disease events, including lessened heart failure pathology and mortality, and including hearts damaged by chemotherapy [60-62]; also decreased mortality from heart attack and lessened atherosclerosis [63-65]
  • Reduced incidence of atrial fibrillation [66]
  • Improved blood pressure control [67]
  • Shortened hospitalizations and surgical recovery rates [68]
  • Reduced thromboembolic (blood clotting) events [69]
  • Improvement in multiple dermatology conditions, including psoriasis [70-72]
  • Significant neuroprotection, including against the pathology in neurological diseases, including Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis [73-75]
  • Improved survival and fewer complications post-stroke, as well as decreased incidence of hemorrhagic and ischemic strokes [76]
  • Emotional and psychological stabilization, with lessened suicide risk [77,78]; decreased neuroinflammation; better management of depression and bipolar disorders, anxiety, cognitive dysfunction, and substance abuse [79]; improved management of substance abuse disorders, including those involving alcohol, cannabis, and tobacco [80-83]
  • Stabilization and symptom improvement in idiopathic intracranial hypertension [84]
  • Improved liver function and lessening of metabolic syndrome [85]
  • Improved lipid metabolism with lessened atherosclerosis formation [86]
  • Improved wound healing in refractory diabetic foot ulcers [87]
  • Lessened hematopoietic stem cell graft rejection [88]
  • Positive clinical impact on autoimmune and autoinflammatory diseases [89]
  • Improved management of polycystic ovary syndrome [90]
  • Improved quality of microvasculature and lessened aneurysm formation [91]
  • No established link with increased cancer incidence, and significant data indicating a decreased incidence [92,93]
  • Reduction in metastatic cancer events in affected individuals [94]
  • Attenuation of breast cancer cell and prostate cancer cell growth [95,96]

Of note, all of the positive effects of GLP-1 receptor agonists cited above are effects that result from increased intracellular levels of vitamin C.

GLP-1RAs, Decreased Appetite/Satiety, and Longevity

As discussed above, GLP-1RAs have been documented to have many different positive impacts on many different conditions. Another way in which these drugs are very positively affecting health and longevity is due to its suppression of appetite and the accelerated appearance of fullness in the stomach (satiety). While it is not clear if or how these effects relate to the glucose-regulating effects of GLP-1RAs, it has been long-established in the scientific literature that decreased calorie consumption increases both longevity and general health. [97-101] The ability of GLP-1RAs to suppress appetite while reaching satiety more rapidly results in chronically decreased calorie consumption. This represents one more reason why these drugs decrease all-cause mortality. Furthermore, it has also been shown that calorie restriction increases insulin sensitivity, which would further promote the positive impact of GLP-1RAs on intracellular VC levels, as discussed below. [102]

The Interaction of Vitamin C with GLP-1 RAs

GLP-1 RAs are both highly beneficial and safe. Nevertheless, side effects of concern are reported in the literature. While the overall impact of GLP-1RAs is enormously positive (decreased all-cause mortality), the ability to deal with and resolve bothersome side effects is always important for the quality of life.

As described above, the levels of intracellular VC determine how healthy cells are. Anything that increases and works to sustain intracellular VC levels will nonspecifically lessen or eliminate any symptomatology.

No symptom can occur in the absence of increased intracellular oxidative stress and decreased intracellular vitamin C levels in the affected cells, tissues, or organs.

The actions of GLP-1RAs increase insulin levels while decreasing the glucagon-mediated release of new glucose from glycogen stores in the liver into the blood. The increased insulin levels with decreased blood glucose levels mean that whatever vitamin C is available in the blood or extracellular spaces will be more readily ushered into the cells since there is less glucose to compete with the increased insulin-induced presence of glucose cell wall transporters. This represents an ideal physiological state in which to increase intracellular VC levels with generous supplementation. Furthermore, the administration of larger amounts of vitamin C more rapidly, as with an intravenous infusion, will further stimulate the pancreas to release even more insulin to push the VC into the cells.

When GLP-1RAs are chronically taken by an individual with low VC intake, both intracellular VC levels and plasma levels of VC will remain low. Low plasma levels of VC trigger an increased release of cortisol from the adrenals in a futile attempt to push VC (that is not sufficiently present any longer) into the cells. When this low VC status is chronic, the increased cortisol blood levels (hypercortisolemia) are chronic as well. Excess cortisol presence also promotes gluconeogenesis, the formation of new glucose from muscle protein. This can result in two significant side effects: muscle wasting (sarcopenia) and a further depletion of intracellular VC levels, since more glucose is available to compete with whatever VC is available for intracellular uptake. Variable degrees of sarcopenia are seen with chronic GLP-1RA treatment. [103,104]

However, when GLP-1RAs are taken with at several grams daily of VC, chronically increased cortisol levels with variable degrees of muscle wasting do not occur. Cortisol levels remain normal, glucose levels are not enhanced, and there is no chronic muscle wasting. Rather, the VC supplementation takes optimal advantage of the enhanced insulin presence (and decreased glucose presence) to chronically keep intracellular VC levels at or near their optimal levels. In fact, in a mouse model of muscle wasting the administration of a GLP-1RA lessens the induced muscular deterioration. [105] Mice, unlike humans, make large amounts of VC in their liver, resulting in muscle tissue protection in the presence of a GLP-1RA drug.

These effects actually make GLP-1RAs powerful anti-aging agents, as nothing is more important to longevity (and quality of life) than optimal levels of intracellular VC. This is further supported by the well-established ability of these drugs to decreased all-cause mortality. Also, VC by itself is also a powerful anti-aging agent. Lower serum VC levels are significantly associated with increased all-cause mortality. [106,107] Taking a GLP-1RA drug while supplementing VC combines two agents that each increase longevity, which will result in a powerful and synergistic anti-aging treatment.

Vitamin C and GLP-1RA: Personal Observations

My personal health problems and their response to hydrocortisone (cortisol) along with vitamin C in getting over and following a severe case of COVID have been previously described. [108] By continuing the hydrocortisone-assisted cellular delivery of my daily VC intake, the many problems that I had most of my life remained minimized but not completely eliminated in the long-term. I also found that temporarily increasing my hydrocortisone assist to my VC supplementation would readily stop a new infection or symptom from taking hold.

Most recently, after starting semaglutide 3 mg daily by mouth, the new improvements in my health have been stunning. My chronic cough that persisted for decades, which had greatly lessened but never disappeared with my hydrocortisone-VC combination, finally completely resolved after roughly the first 10 days of semaglutide. Furthermore, many years of soaking night sweats (etiology unknown) also resolved. One T-shirt now served me well when sleeping, rather than having to change it 3 to 5 times per night. Other less bothersome but nonspecific symptoms have largely resolved as well.

The scientific data and reasoning in this article are clearly consistent with the concept that VC supplementation always helps to some degree with most symptoms. When assisted with hydrocortisone, the response is more dramatic. And, at least for me, it would appear that the addition of semaglutide finally increased intracellular VC levels to the point that all significant symptoms were virtually completely suppressed/resolved. And as with many individuals around the world, my excess abdominal fat is also disappearing quite satisfactorily.

Conclusions and Recommendations

As optimal intracellular VC levels literally define the normalcy of the physiology involved in optimal health, any measure that increases VC inside cells is (or should be) the primary goal of any treatment protocol or supportive health measure. The clinical effects of GLP-1RAs are largely indistinguishable from the clinical effects of sufficiently dosed VC. Furthermore, it is well-established that GLP-1RAs and VC individually lower all-cause mortality. Taken together, the impact is likely additive in nature and probably synergistic in promoting good health while lowering the chances of death. No side effect, unless uniquely severe and incapacitating, should discourage the health seeker from taking a GLP-1RA on a regular basis. And if the side effect is being seen with an injectable form of GLP-1RA, the therapy should not be abandoned without going on a low dose regimen of oral GLP-1RA. And if that causes too bothersome a problem, the half-life of these agents indicates that taking the lowest oral dose on even a less than daily basis would still serve general health well while likely completely eliminating any possible bothersome side effects.

The main downside at this time in taking GLP-1RAs is expense. But even if optimal dosing is not affordable for someone, taking an oral dose even once a week can be expected to provide substantial long-term benefits. Furthermore, as more research is done, intermittent dosing rather than a "steady" binding of GLP-1 receptors in the body might prove to be even more desirable than a relatively continuous binding of the sites with GLP-1RAs. And it would be much more available to low-income individuals.

Recap

Optimal health is achieved when intracellular vitamin C levels can be reached and maintained. Reaching this goal is substantially compromised by the epigenetic defect in most human livers preventing the conversion of glucose to vitamin C in the body. Keeping the cellular VC levels in the body at normal levels in the face of this genetic shortcoming makes reaching optimal health a difficult clinical challenge.

Cortisol (hydrocortisone) and insulin are vital to the ability of cells in the body to achieve normal intracellular levels of VC. The physiological impact of GLP-1RA agents helps to optimize the ability of insulin to bring VC into the cells. And the fact that GLP-1RAs decrease all-cause mortality cannot be ignored or minimized. Decreased all-cause mortality is (or should be) the ultimate goal of any therapy.

Except for the individual who develops intolerable side effects (extremely rare), a GLP-1RA agent, along with a multigram dose of VC, should be taken by everyone in the pursuit of optimal health.

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108. Levy T (2022) https://www.tomlevymd.com/articles/omns20220201/How-COVID-Helped-Me-Regain-Good-Health

 

 

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