Last Updated: Apr 2026
I researched these and found three commonly stated reasons for using such products, which I summarize below. The first intended purpose is exfoliation, or the removal of dead, keratinized skin cells from the epidermis (outer layer) of the skin.1 The second stated purpose is that sugar can act as a humectant, meaning it may help attract and retain moisture in certain formulations.2 The third reason often cited is that some formulations include glycolic acid, a type of alpha hydroxy acid (AHA) that can penetrate the skin and promote exfoliation by loosening the bonds between skin cells, encouraging cellular turnover.3 This type of treatment is commonly referred to as a “chemical peel.”
When I first started researching these products, two questions came to mind: 1. Are these actually beneficial or useful? And 2. Do they truly produce the effects that are claimed? For example, these products are often marketed as making skin appear more youthful by removing the outer layer of skin. But what long-term, unintended consequences might this have on the underlying dermal tissue, where living skin cells reside? The more research I did, the more I realized that the latter question was the more important one to address.
The “conventional wisdom” surrounding these types of products is that they are perfectly safe. However, at Nature’s Complement, we have never been ones to blindly accept conventional wisdom without verifying it for ourselves. We believe part of the value we provide to our customers is the willingness to question common assumptions and take a closer look at what is often accepted without much thought.
In writing this article, we drew on our background in biomedical research, along with our knowledge of biology, chemistry, and health care, to offer a perspective that goes beyond the usual talking points. Our goal is not just to follow trends, but to better understand how these products may impact the skin over time. We hope these ideas help people make more informed decisions and support long-term skin health with longevity in mind.
Cellular Physiology Process Number One
There are two key cellular physiology processes that play roles here. The first is cellular turnover. Most cells in the human body (with some exceptions) have a limit to the number of times they can divide and produce new cells. This limitation is known as the “Hayflick Limit” and is closely associated with the shortening of DNA at the ends of our chromosomes, known as telomeres.4 Due to the nature of DNA replication, each time a cell divides, a small portion of telomeric DNA is lost.
When telomeres become critically short, cells lose their ability to divide and enter a state known as cellular senescence. Senescence can be thought of as a form of cellular “retirement,” where cells remain metabolically active but no longer replicate. Over time, the accumulation of these senescent cells has been associated with various aspects of biological aging, including changes in skin structure and function that contribute to the appearance of aging, such as wrinkles.4
To put this in the context of chemical peels and sugar scrubs, repeated removal of the outer layers of skin can stimulate underlying cells to divide in order to replace what has been lost. Each time a cell divides, a small amount of telomeric DNA is lost, bringing that cell one step closer to senescence.4-6 In theory, frequent and repeated stimulation of cellular turnover could contribute to cumulative telomere shortening over time.
This raises an important question: while these treatments may improve the short-term appearance of the skin by increasing turnover, could excessive or repeated use contribute to long-term changes associated with aging? Cells with longer telomeres are generally considered more biologically “youthful,” and accelerated turnover is not necessarily the same as improved long-term skin health.
That said, it is important to be clear: the direct long-term effects of repeated exfoliation or chemical peels on telomere length in human skin have not been well established. While controlled exfoliation is widely used in dermatology, overuse or misuse may disrupt the skin barrier and lead to irritation or damage.7-9 The concern raised here is whether chronic, repeated stimulation of turnover could have unintended consequences over time.
In other words, while these treatments may help the skin appear smoother or more refreshed in the short term, it is worth considering that more is not always better—especially when dealing with biological systems that have finite limits, such as cellular replication and telomere length.
Cellular Physiology Process Number Two
The second cellular physiology process related to sugar scrubs is known as “non-enzymatic glycosylation,” more commonly referred to as “glycation.” Glycosylation, simply defined, is a process in which a sugar molecule becomes bonded to proteins or lipids. In the human body, enzymatic glycosylation is a normal and essential process, where enzymes intentionally attach sugars to molecules for functions such as cellular recognition and signaling.10 Because this process is enzyme-driven, it is tightly regulated and reversible.
In contrast, non-enzymatic glycation occurs without enzymatic control. In this process, sugars react with proteins or lipids in a largely uncontrolled manner, leading to the formation of compounds known as Advanced Glycation End Products (AGEs).11 These compounds can alter the structure and function of tissues, particularly structural proteins such as collagen, and have been associated with various aspects of aging and disease.11,12
An analogy may help here. A commonly used analogy to explain oxidative damage is when an apple is cut open and turns brown due to exposure to oxygen. Similarly, when sugar is applied to food—such as a sugar glaze on a turkey—and heated, it undergoes browning reactions involving sugars and proteins. While not identical, this is conceptually related to glycation, where sugars chemically modify proteins in ways that can be difficult for the body to fully reverse.
One well-known human condition that involves non-enzymatic glycation is diabetes. If you are diabetic, or know someone who is, you may have heard of the “A1c” or “glycated hemoglobin” test. This test measures the percentage of hemoglobin that has undergone glycation, reflecting long-term blood sugar exposure.13 In other words, it provides an indicator of how much sugar has been interacting with proteins in the body over time.
Diabetics are known to develop numerous secondary complications, many of which are strongly associated with glycation and the accumulation of Advanced Glycation End Products (AGEs).11,13 These include damage to blood vessels, nerves, and connective tissues. It is also well established that individuals with poor blood sugar control often experience impaired wound healing, including in the skin.14 Additionally, glycation-related damage to structural proteins such as collagen has been linked to reduced tissue flexibility and functional decline.12,15
So what does this have to do with sugar scrubs? As the name implies, sugar scrubs involve direct exposure to concentrated sugars. Since high sugar environments can drive non-enzymatic glycation in biological systems, it is reasonable to at least question whether repeated exposure of skin to concentrated sugars could have unintended effects.
That said, it is important to make an important distinction. The outermost layer of the skin, the epidermis, is largely composed of dead, keratinized cells, which limits the likelihood of glycation affecting living tissue at the surface. The question becomes more relevant when considering what happens after exfoliation, when underlying living cells may be more directly exposed.
However, since the main purpose of sugar scrubs is to remove much of the outermost layer of skin, this can result in increased exposure of underlying living skin cells, such as fibroblasts and keratinocytes. This raises an important question: if these cells are exposed to higher concentrations of sugars, could that have unintended effects? While this type of exposure is not typical under normal physiological conditions, whether it leads to meaningful glycation in living skin tissue is not well established.
To be clear, I have not found direct studies specifically examining the effects of topical sugar exposure on living skin cells following exfoliation. That does not necessarily mean the effect is harmless—only that it has not been thoroughly investigated. In fact, the absence of long-term data cuts both ways: there is no strong evidence demonstrating harm, but there is also no solid evidence demonstrating long-term safety or benefit. In other words, claims that these products are beneficial over the long term are, to some extent, based on assumptions rather than direct evidence.
However, there is evidence that Advanced Glycation End Products are involved in skin-related conditions. For example, studies have shown that AGEs can accumulate in psoriatic skin and may contribute to disease processes.16 While this does not directly answer the question of topical sugar exposure, it does reinforce the broader point that glycation can affect skin biology.
There is also substantial evidence in the medical literature that high concentrations of sugar can have harmful effects on a variety of cell types. This includes nerve cells in diabetic neuropathy, vascular and endothelial cells involved in atherosclerosis, and kidney cells affected in diabetic nephropathy.17–19 These effects are often linked, at least in part, to glycation and the accumulation of Advanced Glycation End Products. So the question becomes: why would we assume that skin cells are entirely exempt from similar effects?
Admittedly, this portion of the discussion is more speculative in nature, and I want to be clear about that. However, I have not seen much effort to connect these well-established biological mechanisms to the potential long-term effects of repeated topical sugar exposure on the skin.
The absence of studies on the effects of sugar scrubs does not automatically mean they are safe or without long-term consequences. As the saying goes, “absence of evidence is not evidence of absence.” In many areas of health, it has taken years—or even decades—for subtle but cumulative effects to become fully understood.
So what are my bottom line thoughts on chemical peels, sugar scrubs, and exfoliation? Unless you have a specific need—such as a dermatological condition being managed under professional guidance, or perhaps a rare special event—I would be cautious with the regular use of chemical peels or alpha hydroxy acids. While they can improve the short-term appearance of the skin, repeated stimulation of cellular turnover may not align with long-term skin health.
In other words, occasional use may not be particularly harmful, but frequent or routine use is where concerns begin to arise. When dealing with biological systems that have limits—such as cellular replication and telomere length—it is worth considering whether constant stimulation is truly beneficial over time.
As for sugar scrubs, I would avoid them entirely. They are not necessary, and there are alternative methods to achieve gentle exfoliation if needed. If you feel exfoliation is necessary due to a buildup of dry skin, consider using a soft cloth, a gentle brush, or a coarse soap such as our oatmeal soap.
If you are looking for a humectant effect, I recommend trying our La Rosè lotion which is formulated to support skin hydration.
In the end, while sugar scrubs and chemical peels may offer short-term cosmetic benefits, they are unlikely to provide meaningful long-term advantages—and may, in some cases, work against the goal of maintaining healthy skin over time.
EDIT: We have received requests for additional scientific references on this topic. A partial list of references has been included below, primarily supporting the first portion of this article related to chemical peels and cellular turnover. Additional resources related to sugar scrubs and glycation are provided following the main reference section, and more will be added as research in this area continues to develop.
For Health,
Rob
References:
1. Draelos ZD. Cosmetic Dermatology: Products and Procedures. 2nd ed. Wiley-Blackwell; 2015.
2. Lodén M. Role of topical emollients and moisturizers in the treatment of dry skin barrier disorders. Am J Clin Dermatol. 2003;4(11):771–788.
3. Tang SC, Yang JH. Dual effects of alpha-hydroxy acids on the skin. Molecules. 2018;23(4):863. doi:10.3390/molecules23040863.
4. Hayflick L. The limited in vitro lifetime of human diploid cell strains. Exp Cell Res. 1965;37(3):614–636. doi:10.1016/0014-4827(65)90211-9.
5. Shawi M, Autexier C. Telomerase, senescence and ageing. Mech Ageing Dev. 2008;129(1–2):3–10.
6. Burton DGA, Faragher RGA. Cellular senescence: from growth arrest to immunogenic conversion. Age (Dordr). 2015;37(2):27.
7. Kafi R, Kwak HS, Schumacher WE, et al. Improvement of naturally aged skin with vitamin A (retinol). Arch Dermatol. 2007;143(5):606–612.
8. Fisher GJ, Kang S, Varani J, et al. Mechanisms of photoaging and chronological skin aging. Arch Dermatol. 2002;138(11):1462–1470.
9. Proksch E, Brandner JM, Jensen JM. The skin: an indispensable barrier. Exp Dermatol. 2008;17(12):1063–1072.
10. Varki A. Biological roles of glycans. Glycobiology. 2017;27(1):3–49.
11. Singh R, Barden A, Mori T, Beilin L. Advanced glycation end-products: a review. Diabetologia. 2001;44(2):129–146.
12. Gkogkolou P, Böhm M. Advanced glycation end products: Key players in skin aging? Dermatoendocrinol. 2012;4(3):259–270.
13. American Diabetes Association. Standards of Medical Care in Diabetes—2023. Diabetes Care. 2023;46(Suppl 1):S1–S291.
14. Guo S, Dipietro LA. Factors affecting wound healing. J Dent Res. 2010;89(3):219–229.
15. Haus JM, Carrithers JA, Trappe SW, Trappe TA. Collagen, cross-linking, and advanced glycation end products in aging human skeletal muscle. J Appl Physiol. 2007;103(6):2068–2076.
16. Xue M, Weickert MO, Qureshi S, et al. Advanced glycation end products in psoriatic skin. Br J Dermatol. 2011;164(2):366–372.
17. Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Nature. 2001;414(6865):813–820.
18. Goldin A, Beckman JA, Schmidt AM, Creager MA. Advanced glycation end products: sparking the development of diabetic vascular injury. Circulation. 2006;114(6):597–605.
19. Forbes JM, Cooper ME. Mechanisms of diabetic complications. Physiol Rev. 2013;93(1):137–188.
Additional Scientific Resources:
The following studies and articles provide additional background on telomere biology, cellular senescence, and aging. While not all are directly cited in the text above, they offer further context for readers interested in exploring the underlying science in more detail.
Funk WD, Wang CK, Shelton DN, et al. Telomerase Expression Restores Dermal Integrity to in Vitro-Aged Fibroblasts. Exp Cell Res. 2000;258(2):270–278.
Jaskelioff M, Muller FL, Paik JH, et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature. 2011;469(7328):102–106.
Burton DGA. Cellular senescence, ageing and disease. Age (Dordr). 2009;31(1):1–9.
Levy MZ, Allsopp RC, Futcher AB, et al. Telomere end-replication problem and cell aging. J Mol Biol. 1992;225(4):951–960.
Kimura M, Hjelmborg JV, Gardner JP, et al. Telomere length and mortality. Am J Epidemiol. 2008;167(7):799–806.
Zhu Y, Liu X, Ding X, et al. Telomere and its role in aging pathways. Biogerontology. 2018.
Oeseburg H, de Boer RA, van Gilst WH, et al. Telomere biology in healthy aging and disease. Pflugers Arch. 2010;459(2):259–268.
Blasco MA. Telomere length, stem cells and aging. Nat Chem Biol. 2007;3(10):640–649.
Rode L, Nordestgaard BG, Bojesen SE. Peripheral blood leukocyte telomere length and mortality. J Natl Cancer Inst. 2015;107(6):djv074.
Cawthon RM, Smith KR, O’Brien E, et al. Telomere length and mortality. Lancet. 2003;361(9355):393–395.
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Hi, as a monthly user of Chemical Peels at a clinic which is lead by a Doctor and specialist in Cosmetic Medicine, I felt there was value in sharing with you his response after I sent him a link to your article. I did so because I had some concerns about whether I was doing the right thing, for me and my skin, by having these regular peels, and here is his response to your article.
Kind regards
Therese
Our response to this Doctor’s comments below:
Hello Therese,
Thank you for your interest, and you are right to be concerned. As you mentioned in your follow up email, I’m sure there are many others who are concerned about this also.
What concerns us is that your Dermatologist or other skin Doctor has a key misunderstanding about skin aging, the nature of cellular senescence and cellular aging, and/or ignores a key point of our argument. Therefore his analogies are not appropriate nor correct. He is making justifications for a bad practice, and I explain why below.
The key question that needs to be answered is “what causes skin aging and how does that work?”, and then everything else becomes clear from there. As your Doctor admitted, skin cells, like all cell types that divide frequently, eventually reach cellular senescence or the Hayflick limit. This means there is a limit to the number of times that your skin cells can divide. Your Doctor used the analogy of comparing skin cells to exercising muscles in a gym, but there is a key error here because these work by entirely different physiological mechanisms. Muscles get bigger by a process known as “hypertrophy” – meaning muscles get bigger by growing the size of existing cells larger. Muscles do not get bigger as a result of cellular division (also known as “hyperplasia” in muscles, or “mitosis” in other cell types). Muscles get bigger or smaller by adding or subtracting proteins through a process known as “treadmilling”. This is not how skin is maintained. Skin is maintained through cellular division. Because skin growth and maintenance, and muscle growth and maintenance, are two completely different types of processes, the analogy your Doctor used is incorrect and inappropriate.
A much better analogy for skin cells is the number of times they are able to divide is like a fuse on a bomb – each time a cell divides the fuse gets a little shorter. This “fuse” in cells is know as a “telomere”. Telomeres are a special type of DNA that comprise the ends/tips of the rest of our DNA in our cells. Unlike most of our DNA, telomeres do not contain genes. Telomeres protect the rest of our DNA from getting damaged. So when telomeres get too short, it initiates cellular senescence to prevent cells from dividing further, which would damage DNA that does contain genes. Cells that divide after their telomeres get too short often become cancerous. So instead, cells with short telomeres basically just shut down or die off (through a process known as apoptosis). But eventually you run out of cells that can still divide. When you have a lot of cells that reach senescence and can no longer divide, that is what causes the signs of aging like wrinkles and gray hair.
So when glycolic acid is applied to your skin, as your Doctor admits, it causes cellular turnover or cellular division. As I explained, each time a cell divides, its telomeres get shorter. So by using chemical peels, you are accelerating telomere shortening, and thereby accelerating skin aging. In the long run it will make skin cells reach senescence faster. So later in life you will have more aged skin. This is not speculation, this is strongly supported by the numerous studies I provided. Your Doctor argues that this accelerated turnover is a temporary process, which is technically true. But to go back to my fuse analogy, normally the fuse may be burning slowly, but when you use chemical peels your are accelerating the rate that the fuse burns (albeit temporarily). This makes you reach the endpoint that much faster because you are only born with a certain length of telomeres. Every time a cell divides its telomeres shorten. So by forcing cell division, you are essentially accelerating the shortening of telomeres and accelerating the rate of aging and the rate at which cells will become senescent. Such accelerated turnover does matter. So in the long run this procedure definitely does cause harm and definitely does accelerate skin aging. Because at this time, there are no known methods for re-lengthening telomeres in skin cells, though researchers are trying to do just that. I am extremely certain of all this, as I have spent years researching this topic in the lab.
Your Doctor wrote: “So, if after an initial phase of increased cell turnover your epidermal cells return to a normal degree of turnover, maintaining the new level of epidermal thickness, the whole telomere/Hayflick limit problem no longer exists.”
This is completely incorrect, and shows that your Doctor does not understand modern cellular and molecular physiology of how skin cells age. Returning cellular turnover to baseline only means that the rate by which the fuse is shortening has returned to a slow burn rather than a fast one. That definitely does not mean that the “Hayflick limit problem no longer exists”. The problem is always a consideration, it’s just a matter of how fast you are reaching the problem. So it is aging your skin faster. As stated earlier, each individual is born with a certain length of telomeres, and there is currently no known way to lengthen them. So if you intentionally speed up the process of cellular turnover, you are intentionally speeding up the shortening of telomeres (and aging), as telomeres shorten every time your (skin) cells divide.
Similar problems apply when analyzing your Doctor’s analogy about exercise and free radical generation. Since we live in an oxygen rich environment, human cells have strong mechanisms for quenching free radicals to prevent damage – for example the potent endogenous antioxidant Superoxide dismutase (SOD). Human cells have very little to no ability (depending on cell type) to make telomeres longer. Skin cells normally have no ability to maintain or re-lengthen telomeres. Which means they normally have no way to increase the absolute number of times they can divide. They have no way to make the fuse longer. So again, because the physiological mechanisms are very different, that analogy is also flawed and is inappropriate.
In your more recent email you wrote: “The one particular item of interest to me in the article about the negatives of chemical peels was “about the life span of a cell”. So to answer this concern: by using chemical peels your are accelerating the loss of a cell’s telomeres, which means your are definitely shortening the absolute life span of each affected cell, because they can only divide so many times based on the length of the telomeres. When they run out of telomeres, they can no longer divide. This shortens the lifespan of the cell. This is very straight forward, and is very well documented in the scientific literature.
Your Doctor also wrote: “As an aside, the article you have sent easily moves from supposition to definitive advice. So, on the basis of supposition and speculation he moves almost imperceptibly to statements like “it will cause accelerated skin aging that will definitely become noticeable in your middle or later years”. This statement is based on zero clinical evidence, and mere undergraduate theorising.”
That statement only shows that your Doctor does not understand telomere biology and how skin cells actually age. There are numerous studies (which I have provided that were not Wikipedia articles) which support this conclusion. Your Doctor accused me of quoting Wikipedia articles and not real science. I only refer to Wikipedia for definitions for lay people who may not be familiar with basic concepts. I did also include very relevant peer reviewed studies from NCBI (18+ additional peer reviewed studies at the end of my article). Your doctor attacked my knowledge yet provided zero studies to support his statements, and expects me to accept his statements as fact simply because he has the MD label behind his name. I may not have an MD label, but I am a research scientist, and I can always provide studies to back my statements and arguments.
As an aside, the letters after a person’s name (MD, PhD, MS, BS) are not a good indicator of how much or little they know. I have found that how much someone knows is determined by how much they are willing to learn on an ongoing basis as science advances, rather than what they studied on a one time basis. Doctor’s have a license and a practice to defend because their livelihood depends on it, so investing time in proper research is not practical for them. So instead they do the best they know how with the knowledge that they have, even if it is outdated. If you want cutting edge science, don’t ask a clinician, ask a research scientist. Clinicians don’t have time to keep up with the research literature.
In this case, while there are numerous studies that strongly support the information provided in my original article, in reality, a clinical trial exactly as your Doctor suggests has not been conducted. The key difficulties to properly conducting such a clinical trial are 1. that humans live a long time, so the study would take 20-30 years to conduct, 2. The cost associated with such studies would have a low return on investment due to the length of the study, so finding someone to invest in such a study would be difficult, and 3. there would be ethical and practical difficulties of excluding confounding variables (how do you maintain equal skin exposure to things like UV light and toxins?) So the evidence that your Doctor requires to be convinced is near impossible to acquire, and unfair in the fact that he is not required to provide the same type of long term clinical trial results to show that his treatments do not harm the skin in the long term as he is claiming. He is therefore operating on a double standard. (The limited clinical safety trials on chemical peels have all been short term trials.) The difference here is that he uses his MD label to make statements as facts, while I use research studies to support what I say.
As per your Doctor’s request, I have provided a long list of peer reviewed scientific research papers that support my argument. I am trained as a research scientist, and I worked in pharmaceutical research and development, including pharmaceutical toxicology testing, for well over a decade. I can always support my arguments with extensive research evidence. So your Doctor’s comments were based on inappropriate and inaccurate assumptions. Why did your Doctor not provide peer reviewed scientific research evidence to support the long term safety of chemical peels? Probably because no such research exists?
While it is true that we are selling products, our goal is not to get rich from selling products, but rather to provide healthy alternatives which we also use ourselves. Your doctor is obviously also trying to sell a service, so it seems logically inconsistent for him to criticize us for selling something. The difference is we have provided published, peer reviewed, scientific research evidence that chemical peels are harmful, while your Doctor has not provided any such evidence to support that they are safe in the long term. We would be glad to evaluate any such evidence he may provide.
Please have your Doctor read our response and further explanation. I would be glad to discuss this with him further, at his convenience.
Kind Regards and For Health,
Rob