When we talk about healthy aging, we often think about what we see on the outside: our skin, wrinkles, or other visible signs of aging. But many processes studied in aging research begin much deeper, namely in our cells.1
Each of our cells is surrounded by a membrane, which consists largely of fats. This membrane is far more than just an outer shell. Among other things, it is involved in the cell's transport and communication processes.²
And their fats have a sensitive side: they can be attacked and oxidatively altered by free radicals.
This process is known as lipid peroxidation. The interplay between cell membranes, fats, and oxidative stress is therefore intensively studied in aging research.¹
One vitamin plays a particularly important role: vitamin E, especially in the form of α-tocopherol.
Vitamin E as a chain-breaking antioxidant
Vitamin E differs from many other antioxidants in one crucial aspect: it is fat-soluble. This means it is found in the lipid-rich structures of our body, i.e., where oxidation-sensitive fats are present.
Free radicals are produced naturally during our metabolism. UV radiation, air pollutants, intense physical exertion, or cigarette smoke can further increase their production.1 If their production exceeds our body's antioxidant defense mechanisms, oxidative stress occurs.
Lipid peroxidation can trigger a chain reaction: when one lipid is oxidized, a new radical can be formed that attacks the next lipid. In this way, the reaction can continue indefinitely within lipid-rich structures.²
Vitamin E can interrupt this chain reaction. α-Tocopherol can react with lipid radicals and thereby prevent the oxidative reaction from being passed on to the next lipid.²
Therefore, vitamin E is also referred to in science as a "chain-breaking antioxidant".
This mechanism explains why vitamin E is particularly important for protecting our cells from oxidative stress.
What Vitamin E can change in our skin
This connection is particularly evident in our skin. It is exposed daily to external influences such as UV radiation. This can lead to the formation of reactive oxygen species, which, among other things, oxidatively alter the skin's lipids.
The role of vitamin E in this process was investigated in a human study with 16 healthy individuals. A subset of the participants took 400 mg daily for eight weeks. I.E. α-Tocopherol.³
Afterwards, the vitamin E concentration in her skin had increased from 0.55 to 1.6 ng per mg of protein, almost tripling.
At the same time, the concentration of malondialdehyde decreased significantly.³
This substance is formed during the oxidation of polyunsaturated fatty acids and is therefore used as a marker for lipid peroxidation.
In this study, higher levels of vitamin E in the skin were associated with a lower marker for oxidative changes in its lipids. However, no protection against UV-induced skin reddening was demonstrated.
The results illustrate how closely the skin's vitamin E supply is linked to the biochemical processes surrounding oxidative stress.
Skin and LDL: What connects them
It's not just our skin that contains oxidation-sensitive lipids. LDL, often simply referred to as "bad cholesterol," also transports lipids throughout our body.
LDL plays an important role: it transports cholesterol to various tissues. Cholesterol itself is by no means inherently negative, as our body needs it, among other things, as a component of its cell membranes.
However, the lipids in LDL can also be oxidatively altered.
The Vitamin E Atherosclerosis Prevention Study (VEAPS) investigated this association over an average of three years. Participants received either 400 mg daily. I.E. synthetic α-tocopherol or a placebo.⁴
The result: Vitamin E reduced the concentration of circulating oxidized LDL. At the same time, the susceptibility of LDL to oxidation decreased.
However, no slowdown in the investigated progression of arteriosclerosis was observed.⁴
Skin and LDL initially seem like two completely different topics. But at the molecular level, they are connected by the same process: the oxidative modification of lipids.
Vitamin E does not stop aging. However, it fulfills a scientifically recognized function in protecting our cells from oxidative stress.⁵
Natural and synthetic vitamin E: What is the difference?
Vitamin E is not simply vitamin E.
The term encompasses an entire family of fat-soluble compounds consisting of various tocopherols and tocotrienols. α-Tocopherol plays a particularly important role in humans.⁶
And even with α-tocopherol there is a difference that is hardly visible at first glance.
Naturally occurring α-tocopherol has a clearly defined spatial structure: RRR-α-tocopherol.
Synthetically produced all-rac-α-tocopherol, on the other hand, consists of a mixture of eight different stereoisomeric forms. Only one of these corresponds to naturally occurring RRR-α-tocopherol.⁶
This might initially sound like a detail that would primarily fascinate chemists. However, this spatial structure plays an important role in our bodies.
Our liver contains the so-called α-tocopherol transfer protein. It plays a key role in determining which forms of vitamin E are preferentially released into the bloodstream.
The selective nature of this protein is demonstrated by an investigation of its binding properties: Natural RRR-α-tocopherol was set as a reference at 100 percent. β-Tocopherol reached 38 percent, γ-Tocopherol 9 percent, and δ-Tocopherol only 2 percent.⁷
Studies on humans also show differences between natural and synthetic α-tocopherol.
Following ingestion, natural RRR-α-tocopherol was more highly concentrated in plasma and red blood cells than the synthetic comparator in a pharmacokinetic study.⁸
Natural and synthetic vitamin E may look similar on the label. However, biochemically they are not identical.
Why Vitamin E is so interesting for healthy aging
Skin, cell membranes, lipids, and oxidative stress may seem like disparate topics at first glance. But ultimately, they all lead to the same point: Our cells depend on intact, lipid-rich structures.
And that's precisely where vitamin E plays a special role.
Its ability to interrupt oxidative chain reactions within lipid-rich structures makes α-tocopherol an important component of the body's own antioxidant defense mechanisms.
Those concerned with healthy aging should therefore not only look at the visible signs of aging, but also at the fundamental processes of our cells.
It is worthwhile to take a closer look at the different forms of vitamin E. Natural and synthetic α-tocopherol differ not only in their spatial structure, but also in how they are processed by the body.
Vitamin E thus exemplifies how closely the health of our cells, the protection of their lipids and the biochemical basis of aging are interconnected.
Sources
¹ Pizzino G, Irrera N, Cucinotta M, et al. Oxidative Stress: Harms and Benefits for Human Health. Oxid Med Cell Longev. 2017;2017:8416763.
² Traber MG, Atkinson J. Vitamin E, antioxidant and nothing more. Free Radic Biol Med. 2007;43(1):4–15.
³ McArdle F, Rhodes LE, Parslew RAG, et al. Effects of oral vitamin E and β-carotene supplementation on ultraviolet radiation-induced oxidative stress in human skin. Am J Clin Nutr. 2004;80(5):1270–1275.
⁴ Hodis HN, Mack WJ, LaBree L, et al. Alpha-tocopherol supplementation in healthy individuals reduces low-density lipoprotein oxidation but not atherosclerosis: the Vitamin E Atherosclerosis Prevention Study (VEAPS). Circulation. 2002;106(12):1453–1459.
⁵ Regulation (EU) No 432/2012. Authorised health claim for vitamin E: Vitamin E contributes to the protection of cells from oxidative stress.
⁶ National Institutes of Health, Office of Dietary Supplements. Vitamin E: Fact Sheet for Health Professionals.
⁷ Hosomi A, Arita M, Sato Y, et al. Affinity for α-tocopherol transfer protein as a determinant of the biological activities of vitamin E analogs. FEBS Lett. 1997;409(1):105–108.
⁸ Burton GW, Traber MG, Acuff RV, et al. Human plasma and tissue α-tocopherol concentrations in response to supplementation with deuterated natural and synthetic vitamin E. Am J Clin Nutr. 1998;67(4):669–684.