A question that I am frequently asked is whether peanuts are “okay” or “safe” to eat. The question usually stems from someone who enjoys peanut butter (and there is no replacement, let’s be honest) but has read a lot of conflicting information on the internet and doesn’t know what to think. The idea that peanuts are unhealthy for those without a peanut allergy stems from the canonical paleo diet concept that legumes should be avoided because (1) they aren’t part of our ancestral diet, and (2) they contain toxic anti-nutrients such as lectins and phytic acid.

I’m not going to spend time debating the legume issue because I personally don’t find it very relevant. To me it is a red herring that is brought up by individuals who don’t have an answer specific to peanuts. Moreover, it is a vast overgeneralization to say that one particular legume is unhealthy because some may be harmful. This idea is easily illustrated with simple reduction ad absurdum. If peanuts are unhealthy because they are a legume and some legumes may be harmful, then it would be equally as valid to claim that olive oil is unhealthy because it is a fat and some fats (e.g. trans-fats) may be harmful. Similarly, perhaps we should avoid eating mushrooms altogether because there are some toxic varieties.

The argument from legume doesn’t appear so strong now, does it? Nonetheless, for those who want a more in-depth discussion of the legume issue, I encourage you to check out the presentations and articles put forth by Alan Aragon, Stephen Guyenet, and Chris Kresser.

On the other side of the fence, there are those who habit the use of argumentum ad temperantiam, an argument to moderation. These individuals gravitate towards the middle-ground for whatever reason and assume that the compromise between two positions is always correct. To them, the answer to our question is that having a handful of peanuts or some Nutella on occasion won’t kill you so just enjoy it. Although true, reduction ad absurdum again serves to illustrate why this thought process is wrong. If we replace peanuts with hydrogenated oils or glyphosate, would you still be inclined to say that it is fine to eat in moderation? After all, it won’t kill you, but that doesn’t mean that it is healthy. When people ask about whether peanuts are “safe” to eat, they imply habitual consumption, not a single circumstance.

So let’s judge peanuts as peanuts. Should they be included in an otherwise healthy diet?

What may very well be the first published article to address peanuts directly was a 1998 editorial in the journal Lipids written by Loren Cordain. Conflict of interest aside, the editorial was a response to research conducted by O’Byrne et al. that showed significant reductions of total (-10%) and LDL (-12%) cholesterol in a small group of postmenopausal women consuming a low-fat, high-monounsaturated fatty acid (MUFA) diet based upon peanuts (35-65 g/day for six months). Cordain cautioned that although peanuts *should* be heart healthy through their effects on cholesterol, “there is substantial evidence to indicate that peanut oil, despite its hypolipidemic effects, is highly atherogenic to animals and possibly to humans as well.”

To support his claim, Cordain relies heavily on the work of David Kritchevsky, a true pioneer in dietary fat and cholesterol research. Kritchevsky published a series of articles titled Cholesterol vehicle in experimental atherosclerosis in which he tested how the type of dietary fat consumed influenced the development and progression of atherosclerosis in animal models. Through his experiments, he came across the finding that peanut oil is unexpectedly atherogenic for monkeys, rabbits, and rats, and suggests either the structure of the peanut fat or the lectins present in the peanut oil to be responsible. A decade later, Kritchevsky shows that the more likely cause is the residual peanut lectins that have a high affinity for the smooth muscle cells within the vascular, binding to it and inducing fibromuscular lesions – a necessary precursor for plaque formation.

This is hypothetically a cause for concern, but the practicality is questionable. The majority of Kritchevsky’s experiments were performed with rabbits whose diet was 6% peanut oil (for example), or with monkeys who consumed 14% of their diet as peanut oil (for example). Moreover, the experimental diets were typically a semi-purified mixture of sucrose and casein, which in and of itself adds considerable burden to the body. Assuming the average person eats about two pounds dry weight of food per day, 6-14% peanut oil would equate to 54-127 grams, or 4-9 tablespoons, or 486-1143 kcal PER DAY. Feed this to animals that are adapted to a low-fat herbivorous diet and it isn’t far-fetched to think that problems would ensue.

At this point in time there isn’t any human research on the topic either. After mentioning the work of Kritchevsky, Cordain attempts to draw a connection to human health by forging imaginary relationships and unsupported conclusions from observational data of Indians. His argument distills down to the following:

1. Southern Indians consume more peanut oil than northern Indians.
2. Southern Indians have a higher prevalence of coronary heart disease (CHD) than northern Indians.
3. Therefore, peanut oil is a plausible explanation for the increased heart disease of Southern Indians.

Points (a) & (b) are true, but how point (c) is a rational conclusion is beyond my understanding. Even the study Cordain references makes no mention of peanut oil and instead suggests the cause may be related to the significantly higher rates of smoking seen in the south. But fine, let’s stay focused on possible dietary mediators. According to another study Cordain references, the average Southern Indian diet was composed of 10-30 grams of total fat, primarily from sesame and peanut oil, and a caloric reliance on high-carbohydrate, low-fiber boiled rice, tapioca, or ragi gruel. In contrast, the northern Indian diet was composed of about 75 grams of fat per day from ghee and fermented milk products such as yogurt, and numerous high-fiber carbohydrate sources such as vegetables, whole beans/legumes, and wheat. Not surprisingly, the northern Indians were also much wealthier. Clearly the peanut oil is to blame.

Then, after giving his punch line that peanut oil is a plausible explanation, Cordain immediately throws out a red herring. Specifically, he mentions that olive oil has been consumed for thousands of years, has been shown clinically to reduce the risk of CHD, and that it is superior to peanut oil in terms of its cardiovascular benefits. Therefore, recommending peanut oil is premature for the management of CHD. My first question is who cares? His entire article was about peanut oil, not olive oil, and by quickly switching from his asinine conclusion regarding the Indians to discussing how olive oil is superior for cardiovascular health, Cordain intentionally serves to distract from the relevant and important issue and instead plant seeds that lead readers towards a false conclusion.

Legumes aside, now we know where the canonical paleo-hate for peanuts came from. Personally, I’m not very convinced, especially since it centers on peanut oil and not actual peanuts.

It appears that others feel the same. Cordain’s editorial has been referenced only three times since its publication, all of which are by Cordain himself. Google scholar does list a fourth article from 2005 that was about coconut oil, but checking the reference list shows no mention of Cordain’s editorial. Fortunately the research doesn’t stop where Cordain never took off, so let’s take a look at some other information that is out there.

Peanuts may help regulate blood sugar

Peanut butter rivals apple cider vinegar for reducing the glycemic response to a high-carbohydrate meal in young and healthy adults (figure 1). Specifically, replacing the butter on a bagel with peanut butter reduces the 60-minute glucose response by 56%, which was similar to the reduction (-54%) seen when ~1 tbsp of vinegar was consumed alongside the buttered bagel.

In individuals with type-2 diabetes following a hypocaloric diet, consuming 20% of their daily calories as peanuts, peanut butter, or a combination of both improved the nutrient density of the diet without impacting any of the weight-loss induced benefits on glycemic control or blood lipids. The authors conclude,In obese premenopausal women, the addition of 1.5 ounces (42g) of peanut butter to a wheat-based porridge with orange juice significantly reduced the glycemic response to a white bread and jam lunch meal consumed four hours later and enhanced satiety hormone secretion and reduced the desire to eat. Similar effects were also seen when the women consumed whole peanuts.

“[Peanuts and peanut butter] are convenient, viable and palatable food options that could be easily incorporated into [American Diabetes Association] meal plans prescribed to [type-2 diabetes] patients, and they are compatible with weight management and improvement in specific blood lipids.”

Peanuts are very satiating

Feeding 500 kcal worth of peanuts to free-living healthy adults leads to a strong dietary compensation (i.e. not eating as much of other foods) and increase in resting energy expenditure that together significantly attenuate the predicted weight gain. In other words, the subjects only gained one fourth of the weight that they should have gained by adding 500 kcal into their diets. Importantly, consuming the peanuts for 19 weeks did not alter their pleasantness or hunger ratings, suggesting that they are enjoyable in the long-term.

The importance of whole peanuts on satiety is emphasized by another study that recruited healthy free-living adults from three countries – Ghana, Brazil, and the US, and fed them 30% of their resting energy expenditure (~52g or 460 kcal) as peanut, olive, or safflower oil for eight weeks. The dietary compensation scores were not significantly different between any of the oils, coming in around 45-50% and thus leading to an increased energy intake compared to baseline, and there were also no effects on hunger or desire to eat.

Peanuts may improve cholesterol and triglycerides

Adding 500 kcal of dry-roasted and salted peanuts to the daily diets of healthy & active Ghanaian students without any other dietary restrictions lowered total cholesterol (-8%) and triglycerides (-25%) without increasing energy intake, again supporting the satiating effects of peanut consumption. In fact, 37% of the students were over-compensators that had a reduction in free-feeding energy intake that more than offset the energy contributed by the peanuts, while only 5% were non-compensators. However, when the peanuts were consumed as a snack before bed, thus eliminating the chance for dietary compensation throughout the day, there were no changes in blood lipids. Similarly, when 50% of the subject’s fat intake was replaced by peanuts, the reductions in total cholesterol (-2%) and triglycerides (-8%) were significant but greatly attenuated. Nonetheless, across all study arms, peanut incorporation increased the nutrient density of the diet.

In an experimentally identical study of American adults, similar but different outcomes were seen. Adding 500 kcal of peanuts to the diets of free-living adults had no effect on blood lipids, but triglycerides were significantly reduced when the peanuts were consumed before bed (-24%) and when 50% of the subjects’ fat intake was replaced with peanuts (-17%). Moreover, these changes may be underestimated as the authors mention that,

“Subjects spontaneously commented on the high satiety value of the nuts and reported difficulties with consumption of the prescribed diets; hence, relative to baseline the addition was only 50% of predicted intake.”

Another study of hypercholesterolemic men from Iran found that consuming ~20% of each subject’s usual energy intake as freshly roasted peanuts (ranged from 60-93g or 340-530 kcal) per day significantly increased HDL-cholesterol (+17%) and serum total antioxidant capacity (+13%). The authors calculated the 10-year likelihood of having a heart attack to be reduced by up to 24%. And again, peanuts improved the nutrient density of the diets.

Finally, two studies suggest that the form, flavor, and processing of peanuts do not influence their effects on cardiovascular-related outcomes. One study was an international collaboration that recruited overweight-obese men and women from three countries – Ghana, Brazil, and the US, and fed them56 g (2 oz.) of one of five peanut forms into their diet daily for four weeks. The subjects were allowed to consume them whenever they pleased and no additional dietary instructions were provided. The five peanut forms were whole raw unsalted, whole roasted unsalted, whole roasted salted, whole honey roasted peanuts, and peanut butter. Overall, the only change seen was a significant increase in HDL-c (+6%); however, sub-group analysis showed significant reductions for total cholesterol (-3%), LDL-c (-10%), and triglycerides (-13%) in those with the greatest risk for cardiovascular disease (figure 2). The type of peanut consumed had no effect on anything, leading the authors to ultimately conclude that

“The present study suggests that processing, specifically the addition of flavors, grinding to butter and roasting, does not alter the lipid-lowering effects of peanuts. Significant lipid-lowering effects were observed in hypolipidemic individuals with all peanut varieties. Furthermore, these benefits were achieved without altering body weight status.”

The other study recruited healthy and normal-weight American adults to consume 42g of peanuts (240 kcal salted, honey-roasted, spicy, or unsalted peanuts) into their diets daily for 12 weeks. The subjects were randomized to consume either a single peanut flavor or a combination of three flavors. Reductions in total cholesterol and triglycerides were seen in those subjects with the highest risk of cardiovascular disease only, with no effect of peanut flavor.

Peanuts are nutrient-dense

Many of the studies mentioned previously noted an increase in the nutrient density of the diets the subjects were consuming when peanuts were incorporated. A quick look at the USDA nutrient database shows that peanuts are rich in protein (26% by weight) and dietary fiber (8.5%), both of which may also help explain the reported satiety effects. In fact, peanuts contain more antioxidants per serving than almonds, Brazil nuts, cashews, hazelnuts, macadamia nuts, and pistachios; are considered a major dietary source of resveratrol (1.3-3.7 μ/g) alongside grapes and their derivatives; and possess numerous anti-inflammatory, antitumor, antifungal, antibacterial, and antioxidant effects.

The largest energy component of peanuts is their fat content (49%) which is predominantly unsaturated. Of the total, about 46% is oleic acid and 32% is linoleic acid, which works out to roughly 4.5 grams of linoleic acid per ounce of peanuts. By no means will that do harm, but it isn’t helping anything either. Yet, even this would-be issue is beginning to fade thanks to a 30-year selective breeding experiment headed by Daniel Gorbet of the North Florida Research and Education Center. Over three decades, Gorbert selectively bred different varieties of peanuts to achieve “optimum” attributes. The resulting “SunOleic 97R” is a high-oleic (HO) peanut variety.

In fact, a review dedicated to this high-oleic peanut was published just last year in the International Journal of Food Sciences and Nutrition. What ended up happening with the selective breeding was that the linoleic acid content dwindled down to ~7% while the oleic acid content surpassed olive oil at just over 80%. Actually, its fatty acid profile now resembles that of macadamia nuts. Additionally, from a manufacturing stance, the oxidative stability of peanuts has been found to be 3 to 14-fold greater in the HO variety. Amusingly, it turns out that the O’Byrne study which led Loren Cordain to write his editorial used these HO peanuts.

Interestingly, many benefits appear more pronounced with these HO peanuts as well. In overweight-obese adults, consuming two ounces (56g) of dry-roasted HO peanuts led to a significantly greater increase in resting energy expenditure, diet-induced thermogenesis, and self-reported fullness. In overweight-obese men, consuming two ounces of HO or conventional peanuts in conjunction with a weight-loss diet for four weeks leads to an increase in fat oxidation, and in the HO condition only was there also a reduction in TNF-α. HO and conventional peanuts were also shown to reduce the post-meal rise in plasma lipopolysaccharide (LPS) concentrations characteristic of endotoxemia.

What about the peanut lectin?

As mentioned in the beginning of the article, lectins in general are an argument against legume consumption and I want to stay focused on peanuts specifically. Aside from the animal research using ridiculously high amounts of peanut oil to induce fibrotic lesions in the vasculature, there is a scarcity of research looking into peanuts on this topic after the new millennium. It appears as if the focus shifted from peanut lectins to peanut proteins and allergies. Nonetheless, there is a single study that must be mentioned.

Wang et al. from the University of Liverpool fed two healthy adult volunteers 200g of whole raw peanuts and another five adults 200g of roasted-salted (RS) peanuts in the morning 2-3 hours after a light breakfast. Blood samples were collected for up to 72 hours afterwards for detection of the primary peanut lectin –peanut agglutinin (PNA). As can be seen in the graph below, intact PNA was detected in all five of the people who consumed the RS peanuts and one of the raw peanut consumers, and in vitro studies have shown similar concentrations of PNA stimulate proliferation of epithelial cells. Moreover, hemagglutination activity against red blood cells was detectable as well, confirming that biological activity of the PNA was retained.

This is certainly much stronger evidence than the animal models consuming 4-9 tablespoons of peanut oil daily, but the relevance is still not entirely clear. For starters, the amount of peanuts consumed (200g or 1130 kcal) is unrealistic for most people, and even with this amount there was a return to baseline levels by four hours in all but one of the subjects and by 24 hours in everyone. How much damage is done with this transient elevation is unknown, but my guess would be not much, especially considering the animal models consumed their peanut oil throughout the day on a daily basis for weeks. Would you eat 200g or 1130 kcal of peanuts every four hours for a month?

What about Aflatoxins?

Aflatoxins are definitely a healthy concern and can indeed be fatal. These mycotoxins are produced by some fungi and mold (Aspergillus flavus and Aspergillus parasiticus), and colonize/contaminate grain and groundnut crops before harvest or during storage. However, the U.S. government places regulations on the aflatoxin concentration of peanuts, requiring them to be below 15 parts per billion. So although detectable quantities of aflatoxin have been found on Chinese peanut butter, this doesn’t apply to American brands. In fact, an analysis of the risk of liver cancer in the USA associated with aflatoxin ingestion from peanuts found that for the male Fischer rat, the most sensitive mammalian species studied, an estimate of 158 cases of liver cancer per year in the USA at could be attributed to the current levels of aflatoxin exposure. Granted this study was conducted in 1984, but it serves to show how US regulations have since hammered down on aflatoxins and made them of little concern to peanut consumers.

When people would ask my opinion on the peanut issue, I never had a satisfactory answer, and that was my fault. But now I do. The fundamental issues presented by Cordain and accepted as dogmatic fact are a stretch to say the least, and from a practical standpoint, are not likely to translate to humans. The concerns regarding PNA are over-exaggerated and restricted to animals consuming unrealistic amounts of concentrated peanut oil. Similarly, concerns about aflatoxins are warranted but not likely an issue in the U.S.

Peanuts are a nutrient dense food that consistently shows benefits in some cardiovascular disease risk factors such as triglycerides and cholesterol, especially in those who are at the greatest risk. Additionally, peanuts may hold promise as an anti-diabetic aid and if anything will at least leave you feeling full and satisfied. Although other nuts may have a more favorable fatty acid profile over the conventional peanut, there does exist the high-oleic peanut variety that is just as good as olive oil or macadamia nuts.

So I say TO PEANUT!