Vinpocetine And Blood Flow To The Brain — What The Evidence Shows
Quick Read Vinpocetine is a supplement derived from the periwinkle plant that has been used clinically in Europe and Asia
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Simon Parrott – Vitacuity Ltd
In 1929, researchers discovered that certain fats are essential, meaning your body cannot make them and must get them from food. When they fed rats a diet with no fat, the animals developed scaly skin, stopped growing, lost the ability to reproduce, and died. When fat was reintroduced, they recovered. This finding launched nearly a century of research into omega-3 fatty acids, which your body uses to build cell membranes, control inflammation, and create signalling molecules that manage blood clotting and immune responses.
A major breakthrough came in the 1970s when researchers studying Greenlandic Inuit people noticed they had very low rates of heart disease despite eating large amounts of fat from marine sources. The researchers found that a specific omega-3 fatty acid called EPA, abundant in fish, prevented blood clots from forming too easily, protecting against blocked arteries. This sparked widespread scientific interest in omega-3s that continues today. A 1987 human study of tube-fed patients confirmed that omega-3 deficiency causes scaly skin and other problems that disappear when the fatty acids are restored.
Modern research shows that omega-3 and omega-6 fatty acids must be balanced, but most diets today are skewed too far toward omega-6 from seed oils. Plant-based omega-3 sources like flaxseed and walnuts provide some benefit, but the real health effects come from long-chain omega-3s called EPA and DHA, found mainly in oily fish or marine supplements. Your body can convert the plant version into these forms, but the process is inefficient.
Verdict: Omega-3 fatty acids are genuinely essential for health, and for most people eating modern diets, supplementation with fish oil or algae-based omega-3s containing EPA and DHA is a safe, practical, and evidence-supported choice.
In 1929, two researchers made a finding so simple, so unexpected, that it quietly rewrote the rules of human nutrition. George and Mildred Burr, working at the University of Minnesota, fed rats a diet completely stripped of fat. The prevailing wisdom of the time said this shouldn’t matter much, fat was considered little more than a calorie source, a fuel you could theoretically replace or remove. What happened next was startling. The rats developed severe scaly skin, failed to grow, lost reproductive function, and eventually died. When the Burrs reintroduced specific fats to the diet, the animals recovered. Their conclusion, published in the *Journal of Biological Chemistry*, was radical for its era: certain fats are not optional. They are essential. The body cannot make them. You must eat them.
That discovery, now nearly a century old, planted the seed of everything we understand today about omega-3 fatty acids, inflammation, brain health, and heart disease. Here’s what decades of research has taught us, and where that extraordinary journey has taken us.
The term “essential” in nutrition has a precise meaning. It doesn’t just mean important. It means the body genuinely cannot synthesise the compound from scratch, it must come from food. The Burrs identified linoleic acid (an omega-6 fatty acid) as the first essential fatty acid in 1930, and shortly after, alpha-linolenic acid (ALA, an omega-3) was also shown to prevent the fatty acid deficiency syndrome in animals [3].
Think of these fatty acids as molecular raw materials. Your body uses them to build cell membranes, regulate inflammation, and produce a family of powerful signalling molecules, prostaglandins, thromboxanes, prostacyclins, and leukotrienes, that govern everything from blood clotting to immune response [4]. Without the right fats in your diet, these systems begin to fail in ways that are visible (scaly skin, hair loss) and invisible (compromised immune signalling, impaired organ function) [6].
The omega-3 family has a parent molecule, ALA, which acts as a precursor to two longer-chain fatty acids that have become the focus of modern research: EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) [8]. DHA in particular has been conserved in neural signalling systems across hundreds of millions of years of evolution, from cephalopods to fish to primates to humans, a remarkable fact that speaks to how fundamental this molecule is to brain function [8].
But here is where the story gets more complicated, and more interesting.
For several decades after the Burrs’ original discovery, omega-3 fatty acids were something of an afterthought. Interest faded partly because some prominent laboratories in the mid-20th century struggled to replicate findings showing that ALA alone could prevent deficiency symptoms [3]. The omega-3 family was overshadowed by its omega-6 cousins.
The turning point came in the 1970s. Danish researchers Dyerberg and Bang published findings that stopped the lipid research community in its tracks. They had been studying the Greenlandic Inuit, a population with a diet extraordinarily rich in marine fats, and noticed something remarkable: despite eating large quantities of fat, the Inuit had strikingly low rates of atherosclerotic coronary disease [3].
Dyerberg and Bang went further. They found that EPA, the long-chain omega-3 abundant in marine lipids, was elevated in Inuit plasma, and that it inhibited platelet aggregation. Platelets are the clotting agents in your blood; when they aggregate too readily, you’re at higher risk of arterial blockages. The researchers concluded that the anti-thrombotic (anti-clotting) effect of EPA was protecting the Inuit against coronary artery disease [3].
This was the spark. It ignited widespread scientific interest in EPA and DHA that has not dimmed since, ultimately leading to the present understanding that omega-3 fatty acids are genuine essential fatty acids with critical physiological roles, not just in the heart, but across multiple systems [3].
*Evidence grade: This Inuit observational finding is historically strong as a hypothesis-generator, though it should be understood as epidemiological, it identified the pattern, not the mechanism. Subsequent research has built the mechanistic picture.*
It is one thing to show deficiency in rats. It is another to demonstrate it in people. A particularly compelling piece of human evidence came from a 1987 clinical study of four adults being fed exclusively by gastric tube over a long period [15]. Their tube-feeding formula lacked alpha-linolenic acid, and the consequences were measurable and clear.
In blood plasma and red blood cells, total omega-3 fatty acids dropped significantly, including ALA, EPA, and DHA. The patients developed a mild but definite scaly dermatitis. When essential fatty acid supplementation was introduced, the skin condition resolved, and omega-3 levels in plasma and red blood cells normalised [15].
This study also provided one of the first human estimates of how much omega-3 we actually need at a minimum: approximately 0.2–0.3% of total energy intake from linolenic acid, and 0.1–0.2% from long-chain omega-3s such as EPA and DHA [15]. Small amounts, but apparently non-negotiable.
*Evidence grade: Promising, small sample (4 patients), but compelling as direct human evidence of deficiency and recovery.*
One of the most important, and frequently overlooked, insights from a century of fatty acid research is that omega-3 and omega-6 fatty acids don’t operate independently. They interact, compete, and must be balanced [1].
Omega-6 fatty acids, particularly linoleic acid and arachidonic acid, are physiologically important. They are not the enemy. But their consumption needs to be balanced with long-chain omega-3 fatty acids [1]. The trouble is that modern diets, especially those high in seed oils, have dramatically shifted this balance towards omega-6, partly as a result of official dietary guidelines over the past century that encouraged increased consumption of seed-derived fats while discouraging traditional fats [1].
Research from 2023 flags a nuance that often gets lost: ALA, the plant-based omega-3 found in flaxseed, walnuts, and chia seeds, has “rather limited use as an anti-inflammatory agent,” a fact that is frequently overlooked in popular nutrition writing [1]. The real action, as far as the evidence goes, lies with the long-chain omega-3s: EPA and DHA. ALA must be converted by the body into EPA and DHA to exert most of its meaningful effects, and that conversion is inefficient in humans [8].
This is a practical point worth understanding. Eating more flaxseed is not the same as eating oily fish. Both provide omega-3s, but not equivalently.
*Evidence grade: Strong for the importance of the omega-3/omega-6 balance. Promising to strong for ALA conversion limitations, consistent across multiple papers.*
The skin was, in many ways, the original diagnostic tool for essential fatty acid deficiency, and it remains instructive today. Research from 1987 demonstrated in animal models that deficiency of linoleic acid (the omega-6 essential fatty acid) causes severe scaly dermatosis, excessive water loss through the skin, and hyperproliferation of the epidermis [6]. Reintroducing linoleic acid or gamma-linolenic acid reversed these symptoms.
Interestingly, fish oil, containing EPA and DHA, did *not* reverse the skin deficiency symptoms caused by lack of omega-6 fatty acids [6]. This finding underlines a key principle: omega-3 and omega-6 fatty acids have distinct, non-interchangeable roles. They modulate each other’s metabolism, but they are not substitutes for one another [6].
The skin findings matter beyond dermatology. They illustrate how fatty acid deficiency manifests systemically, in organ function, membrane integrity, and the body’s ability to regulate water and inflammation. When researchers in 1984 were still refining experimental designs to study essential fatty acid deficiency in rats [10], and when 1977 and 1978 studies were quantifying how much gamma-linolenic acid was needed to reverse deficiency [11, 13], the picture emerging was consistent: these fatty acids are not optional extras. They are structural and functional necessities.
*Evidence grade: Strong for the essential role of omega-6 (linoleic acid) in skin integrity. Early stage to promising for specific omega-3 skin effects.*
The cardiovascular chapter of omega-3 research is, frankly, one of the most debated in nutritional science [12]. And it’s worth being honest about why.
A 2020 review published in *Nutrients* describes fatty acids in the context of cardiovascular disease as “one of the most controversial areas of nutrition research” [12]. The reason for the conflict is not that the science is bad, it’s that the science is genuinely complex. Dietary fatty acids incorporate into cell plasma membranes, altering fluidity and physiological function. They reshape the availability of eicosanoids and other lipid mediators that direct inflammation and stress responses [12]. These are not simple linear effects that one randomised trial can fully capture.
Why do studies conflict? The 2020 review identifies several reasons [12]: studies vary by the type of fatty acid tested, the dose used, the background diet of participants, the population studied, and the era of medicine in which the trial was conducted. A trial done in the 1980s on a population eating a very different diet from today cannot be directly compared to a modern trial. Different doses produce different effects. And “fatty acids” is not one thing, EPA and DHA behave differently from ALA, from linoleic acid, from saturated fats.
The weight of evidence, however, is not directionless. A 2023 paper is clear that the targeted use of long-chain omega-3 fatty acids, EPA and DHA, based on blood analysis “has great potential to supplement or even be an alternative to various pharmacological therapies” [1]. That is a careful, measured statement, but it is a significant one from researchers who reviewed the full landscape of fatty acid science.
*Evidence grade: Conflicted, but conflicted because of complexity, not because omega-3s lack effect. The nuanced conclusion is that long-chain EPA and DHA at appropriate doses have real cardiovascular relevance.*
A century of fatty acid research has taught us an enormous amount, but the honest answer is that several important questions remain open.
ALA’s intrinsic role is still undefined. We know ALA is the parent omega-3 and that it converts to EPA and DHA. But whether ALA has important biological functions of its own, independent of its conversion products, is genuinely unclear [8]. Rat and mouse studies aren’t reliably translatable to humans here because rodents convert ALA to EPA and DHA far more efficiently than we do [8].
How much omega-3 do we actually need? The 1987 human tube-feeding study gave us minimum estimates [15], but optimal intake, as opposed to merely sufficient intake, for cognitive health, cardiovascular protection, and healthy ageing is still being debated. Individual variation is real.
The omega-3 index as a clinical tool. The concept of testing blood omega-3 levels to guide supplementation is promising [1], but it remains underused in standard clinical practice. Whether routine testing would meaningfully improve health outcomes at a population level requires more large-scale evidence.
Long-term supplementation trials. Many omega-3 trials have been relatively short in duration. The long-term effects of sustained EPA and DHA supplementation on ageing, cognition, and cardiovascular outcomes, across diverse populations and dietary backgrounds, still need larger, longer studies.
The conversion problem. For people eating plant-based diets who rely on ALA from flaxseed and walnuts, the question of whether conversion to EPA and DHA is sufficient for optimal health is unresolved. Some evidence suggests it is not [1, 8], but we don’t have definitive human trial data on this.
Here is what a sensible, informed person should take from 95 years of essential fatty acid research.
Fat is not the enemy, the *type* of fat is what matters. The Burrs proved this in 1929, and every decade of research since has reinforced it. The modern fear of dietary fat, driven by guidelines that encouraged seed oils and discouraged traditional fats, may have inadvertently disrupted the omega-3/omega-6 balance that our biology depends on [1].
ALA from plant sources is valuable but not sufficient for most people. Flaxseeds, walnuts, and chia are worth eating. But if you want the benefits that the research actually points to, reduced platelet aggregation, anti-inflammatory effects, cardiovascular protection, you need EPA and DHA, and those come from oily fish or marine-sourced supplements [1, 3].
Omega-3 supplementation is safe, practical, and the case for it is strong. EPA and DHA are not fat-soluble in the way that creates toxicity risk at normal doses. The research consistently shows that deficiency is common, that its effects are real, and that supplementation corrects it. A high-quality fish oil or algae-based omega-3 supplement (the latter particularly relevant for those avoiding fish) is one of the most evidence-supported supplements available.
Balance matters as much as quantity. You don’t just need more omega-3, you need to think about your overall omega-6 intake too. Cutting back on highly refined seed oils while ensuring adequate EPA and DHA is a more complete strategy than simply adding fish oil to an otherwise unchanged diet [1].
If you want to be precise, consider testing your omega-3 index. Blood testing for omega-3 status exists and is available privately in the UK. It tells you where you actually are, rather than guessing. If testing feels impractical or too costly, supplementing with a quality EPA/DHA product daily is a safe, rational default, the risk of deficiency almost certainly outweighs any risk of supplementing at normal doses.
The journey from two researchers and a group of fat-deprived rats in 1929 to our current understanding of omega-3s and human health is one of science’s quiet triumphs. It moved slowly, hit dead ends, sparked controversies, and produced genuine disagreements, because that is what real science does. But the direction of travel has been consistent. These fatty acids are essential. They matter for your heart, your brain, your skin, your cellular membranes, and your inflammatory response. And the gap between what most people consume and what the research suggests is optimal is, for many of us, worth closing.
At Vitacuity, we analysed over 1.77 million research papers to bring you the most relevant evidence on this topic. The findings above represent the clearest picture the science currently supports.
[1] Fatty acids: facts vs. fiction. (2023). *Annals of Nutrition and Metabolism.* DOI: 10.1024/0300-9831/a000713 | https://pubmed.ncbi.nlm.nih.gov/34041926/
[2] Omega-3 Fatty Acids: Not Really Fishy; Lessons Learned. (2024). https://pubmed.ncbi.nlm.nih.gov/38268497/
[3] Emergence of omega-3 fatty acids in biomedical research. (2019). *Prostaglandins, Leukotrienes and Essential Fatty Acids.* DOI: 10.1016/j.plefa.2018.11.017 | https://pubmed.ncbi.nlm.nih.gov/30553403/ | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6362845/
[4] Significance and motivation of the clinical use of essential fatty acid derivatives, especially gamma-linolenic acid. (1990). https://pubmed.ncbi.nlm.nih.gov/2158408/
[5] Essential fatty acids in the liver and adipose tissue of genetically obese mice: effect of supplemental linoleic and gamma-linolenic acids. (1985). https://pubmed.ncbi.nlm.nih.gov/2998443/
[6] Biologic significance of polyunsaturated fatty acids in the skin. (1987). https://pubmed.ncbi.nlm.nih.gov/3688908/
[7] The effect of dihomo-gamma-linolenic acid (20:3,n-6) on the composition of phospholipid fatty acids in the liver of rats deficient in essential fatty acids. (1978). https://pubmed.ncbi.nlm.nih.gov/666999/
[8] Past and Present Insights on Alpha-linolenic Acid and the Omega-3 Fatty Acid Family. (2016). *Critical Reviews in Food Science and Nutrition.* DOI: 10.1080/10408398.2013.828678 | https://pubmed.ncbi.nlm.nih.gov/25774650/
[9] Reply to Hansen: Essentiality of n-3 fatty acids. (2019). *Journal of Biological Chemistry.* DOI: 10.1074/jbc.RL119.008526 | https://pubmed.ncbi.nlm.nih.gov/31028162/ | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6497932/
[10] Essential fatty acid deficiency: a suggestion concerning experimental design. (1984). https://pubmed.ncbi.nlm.nih.gov/6608589/
[11] Potency of gamma-linolenic acid (18:3omega6) in curing essential fatty acid deficiency in the rat. (1977). DOI: 10.1159/000176158 | https://pubmed.ncbi.nlm.nih.gov/917383/
[12] Fatty Acids and Cardiovascular Risk. Evidence, Lack of Evidence, and Diligence. (2020). *Nutrients.* DOI: 10.3390/nu12123782 | https://pubmed.ncbi.nlm.nih.gov/33317164/ | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7764656/
[13] Metabolism of gamma-linolenic acid in essential fatty acid-deficient rats. (1977). https://pubmed.ncbi.nlm.nih.gov/845689/
[14] Essential fatty acids, their metabolism and interrelationships. (1970). https://pubmed.ncbi.nlm.nih.gov/4943639/
[15] Alpha-linolenic acid deficiency in patients on long-term gastric-tube feeding: estimation of linolenic acid and long-chain unsaturated n-3 fatty acid requirement in man. (1987). https://pubmed.ncbi.nlm.nih.gov/2879436/
This article is for informational purposes only and does not constitute medical advice. Food supplements should not be used as a substitute for a varied and balanced diet and healthy lifestyle. If you are pregnant, breastfeeding, taking medication or have a medical condition, consult your doctor before taking any supplement. These statements have not been evaluated by the Food and Drug Administration (FDA) or the Medicines and Healthcare products Regulatory Agency (MHRA). This product is not intended to diagnose, treat, cure, or prevent any disease.
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