There are many dessert recipes on line containing cups and cups of nuts claiming to be full of ‘healthy fats’. This led me to wonder are the fats in nuts really so healthy? Nuts are extremely high in calories and the majority of these calories come from monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs). You hear a lot in main stream media about MUFAs and PUFAs being ‘heart-healthy’ and it occurred to me that I honestly don’t know too much about why these fatty acids are considered ‘healthy’. I also wondered what are the mechanisms accounting for these so-called health benefits? So I did some research, particularly focusing on the relationship between the fats in nuts and cardiovascular health.
Nuts contain a high amount of fat ranging from 46% in cashews and pistachios to 76% in macadamia nuts (1). This fat is predominantly in the form of MUFAs. Hazelnuts, for example, contain approximately 61% total fat content with approximately 90% of those fats being the MUFA oleic acid (45.7 grams/100 grams) (2, 3). Nuts also contain PUFAs; the omega-6 or n-6 PUFA linoleic acid and the short chain omega-3 or n-3 PUFA α-linolenic acid (ALA). Walnuts are in fact the whole food with the highest content of ALA of all edible plants (1). Nuts are reported to have many health benefits. Before I go on, allow me to define exactly what nuts are. Tree nuts are dry fruits with one seed. Peanuts are actually legumes but have a similar nutrient profile to tree nuts. Chestnuts are unlike other tree nuts as they are starchy and contain little fat.
The first reports of the cardiovascular health benefits of nuts
The first reports of the health outcomes of nuts was in the early 1990s when two important studies were published: the Adventist Health Study, which related frequent nut consumption with a lower risk of coronary heart disease (4) and a randomized clinical trial showing that the intake of walnuts reduced serum cholesterol levels (5). The clinical trial was published in 1993 and involved 18 normal men aged between 21 and 43 weighing between 60kgs and 103kgs. The subjects all started the study consuming a reference diet for five days. After this one group followed the walnut diet for four weeks followed by the reference diet for four weeks while the other group followed the reference diet for four weeks followed by the walnut diet for four weeks. The composition of the reference diet and the walnut diet were basically identical with respect to their total calories, fat, protein, carbohydrate and fiber. The study states the following: ‘The foods in the walnut diet were identical to those in the reference diet; however, the portions of fatty foods, such as potato chips and meat, were reduced, and the amount of visible fat (oils, margarine and butter) was decreased to accommodate the percentage of calories derived from walnuts (20 percent).’ The results from this study suggest that replacing a portion of the fat in one’s diet with walnuts without increasing the percentage of calories from fat will reduce serum cholesterol levels and favourably modify the lipoprotein profile in healthy men (5). However, when you look at the food that the walnuts replaced ie. fatty foods, such as potato chips and meat, my thoughts were perhaps it was the removal of these items rather than the incorporation of the walnuts that produced the beneficial outcomes.
Studies investigating the cardiovascular health benefits of nuts
Since then many epidemiological and random clinical trials have been conducted on nut consumption and cardiovascular health. Large studies conducted in the US investigating associations of dietary components with health outcomes reported a beneficial effect of nut consumption on fatal and non-fatal coronary heart disease (CHD) after a follow-up period ranging from 6 – 18 years (6-8). A more recent report involving two large cohorts of men and women (the Nurses’ Health Study and the Health Professionals Follow-up Study) again found reduced CHD mortality for both sexes with increasing nut consumption (9). In this particular study, nut consumption was also associated with a reduction in all causes of death and cancer mortality. The results from these studies suggest a strong association (not direct causation) between nut consumption and reduced CHD rates. There is also some epidemiological evidence that frequent nut consumption is associated with a protective effect from metabolic syndrome (10, 11), hypertension (12, 13) and reduced circulating levels of inflammatory biomarkers (14, 15), which may be predictors of CHD.
In 2010 an analysis of 25 random clinical trials conducted in seven countries examining the impact of nut consumption on blood lipid levels was performed (16). The trials included in this analysis ranged from 3-8 weeks and included 583 men and women with normal lipid levels and high cholesterol levels (hypercholesterolemic) who were not taking lipid-lowering medications. The types of dietary interventions used in the 25 clinical trials were as follows: subjects consumed nuts without dietary advice, subjects were given dietary advice and a biological measure was used to ensure that subjects were following the diet or subjects were provided with nuts and all meals.
The analysis showed that nut consumption had a cholesterol-lowering effect. In more detail, it was found that the consumption of 67 grams of nuts per day (that’s about 60 nuts depending on the nut) was associated with an average reduction in total cholesterol, a reduction in low-density lipoprotein-cholesterol (LDL-C) (the ‘bad’ form of cholesterol) and a reduction in the ratio of LDL to high-density lipoprotein (HDL). It was also found that the cholesterol-lowering effects of nuts were greater for subjects who started the study with higher LDL-C levels and a lower body mass index (BMI), and for those subjects following a typical Western diet rather than a Mediterranean diet. In other words, if you are not obese but have high LDL-C levels and are following a Western diet, consisting of predominantly refined cereals and sugars, refined vegetable oils, fatty meats, dairy products and salt (17), then you will benefit the most from substituting calories from saturated fats with nuts.
It seems to me that in a lot of these studies nuts are being substituted for other components in the diet while keeping the amount of calories consistent. Again this makes me think that perhaps it was not the inclusion of the nuts that was causing these positive health benefits but rather the elimination of other food components, such as refined carbohydrates combined with saturated fats. It should also be noted that nuts contain other potentially beneficial compounds, such as plant sterols, which may contribute to the cholesterol lowering effects. I believe that the take home message from this analysis is that if you are hypercholesterolemic and are eating a pretty awful diet consisting of high levels of refined carbohydrates and saturated fats, then substituting some of these foods with nuts may lower your total cholesterol and your LDL-C, which is considered a marker for cardiovascular disease (CVD). Even better advice would be to eliminate these foods altogether.
What are the mechanisms for the potential cardiovascular health benefits of nuts?
I next wondered what were the possible mechanisms accounting for the reduction in CVD risk factors associated with nut consumption? Nuts are rich in unsaturated fatty acids. Most contain high amounts of MUFAs, but walnuts are especially rich in both omega-6 or n-6 (linoleic acid) and omega-3 or n-3 (α-linolenic acid) PUFAs. So I did some research into the effects of the different types of fatty acids on human cardiovascular health.
A brief overview of triglycerides, fatty acids and lipoproteins
Firstly, let me give you a brief introduction to triglycerides (TGs) and fatty acids in the human diet. TGs are the main source of fat in the human diet and are made up of a glycerol backbone (an alcohol with multiple hydroxyl groups for the chemists out there) and three fatty acids. These fatty acids vary in chain length from 2 carbons to 24 carbons, referred to as short-, medium- or long-chain fatty acids, and can be saturated or unsaturated fatty acids. The first step in the digestion of TGs is the partial breakdown into diacylglycerols and free fatty acids, which occurs in the stomach via the actions of the enzymes gastric lipase and lingual lipase. This predigestion in the stomach assists fat digestion in the first part of the small intestine, the duodenum. The entry of TG degradation products into the duodenum triggers the secretion of pancreatic lipase and the release of bile acids from the gall bladder or from the liver. The combination of bile acids and pancreatic lipase results in the complete breakdown of TGs into monoacylglycerol and free fatty acids. Fatty acids can also be made in the human body, except for the essential fatty acids; these must come from the diet (18).
Now let’s move on to lipoproteins. The synthesis and secretion of lipoproteins by the intestinal absorptive cells (enterocytes if you want to sound smart) is necessary for the transportation of dietary lipids or fats in the blood stream and to deliver these lipids to other tissues in the body. This is because TGs and cholesterol are virtually insoluble in plasma and must be transported in the human body as lipoprotein particles. Lipoprotein particles consist of a lipid component made up of cholesterol, cholesterol esters, phospholipids and TGs (free fatty acids are reassembled into TGs once inside the enterocytes) and a protein component. Lipoproteins are divided into seven classes based on size, lipid composition and protein composition (chylomicrons, chylomicron remnants, very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), LDL, HDL and Lipoprotein (a)). Chylomicrons are the first lipoprotein particles formed in the intestinal enterocytes. They are then delivered to the blood stream where the chylomicrons can deliver TGs to the adipose tissue and muscles for energy and storage. The size of chylomicrons can vary depending on the amount of fat ingested. Once TGs have been removed from chylomicrons in adipose and muscle tissues, they become chylomicron remnants. The chylomicron remnants are taken up by the liver, where they are formed into VLDL. VLDL can be further metabolized to IDL and LDL (19).
Apoproteins (apo) or apolipoproteins are the protein component of lipoprotein particles. Apoproteins are critical in the regulation of lipid transport and are also involved in lipoprotein assembly and lipid metabolism by interacting with enzymes, lipid transport proteins and receptors (put simply receptors are proteins, often on the surface of cells, that bind signalling molecules and transmit these signals).
Apolipoprotien B (apoB) exists as two forms: apoB-100 and apoB48. ApoB-100 is formed in the liver and assembles in to VLDL, which are later converted to LDL. ApoB48 is formed in the intestine and is essential for the assembly of chylomicrons. ApoB100 contains basic amino acids that become positively charged and interact with the negatively charged sulfate groups of the proteoglycans (glycosylated proteins) on the artery wall. This results in an accumulation of LDL in the arterial wall leading to atherogenic plaques (20, 21). This is one of the reasons why LDL-C is considered the ‘bad’ form of cholesterol.
On the other hand, Apolipoprotein A-1 (apoA-1) is the major protein component of high-density lipoprotein (HDL) particles. Why are HDL particles considered ‘good’ cholesterol? One reason is that HDL particles are involved in reverse cholesterol transport (RCT). RCT is the process whereby cholesterol is transported from the peripheral tissues, such as the cells in the arterial walls, to the liver by HDL particles to be used in other lipoproteins and for the synthesis of bile acids, steroid hormones and fat-soluble vitamins (22).
Saturated fatty acids (SFAs) and cardiovascular health
Saturated fatty acids are found in palm oil, coconut oil, cocoa butter and animal-derived fats. Dairy fats also contain some odd-chain saturated fatty acids (pentadecanoic acid and hexadecanoic acid). There is evidence, mostly in animals, that the major dietary saturated fatty acids (lauric, myristic and palmitic acid) can raise total and LDL-C by suppressing LDL receptor activity in the liver, leading to a reduced rate of LDL clearance. Saturated fatty acids may also increase LDL production rate (23-25). There is also evidence that saturated fatty acids increase coagulation (blood clotting), induce insulin resistance and promote inflammation, however the results are not consistent on all of these effects (26).
I was fascinated to learn that the latest research in the field of nutritional science shows that fatty acids and dietary fats influence gene expression. This means that fats consumed from the diet can cause certain genes to be switched on or off and control the proteins produced by cells in the human body. One way that fatty acids can influence gene expression is by acting on transcription factors. Transcription factors are proteins that bind to specific sequences of DNA and control the rate of transcription of genetic information. Saturated fatty acids can influence genes involved in the synthesis and metabolism of cholesterol, fatty acids, triacylglycerols and phospholipids, and the assembly, secretion and clearance of lipoproteins (27). It has been shown that saturated fatty acids may increase the secretion of very low-density lipoprotein (VLDL) (28). VLDL is one of the atherogenic particles carrying cholesterol, meaning that it contributes to CVD (29).
The research suggests that the replacement of common saturated fatty acids with dietary MUFAs or with PUFAs has beneficial cardiovascular outcomes, in particular the lowering of blood cholesterol and LDL-C (30). Now, this is where the research becomes a little hazy. It was once believed that dietary saturated fatty acids were responsible for increased LDL-C and hence CVD. However, it is becoming clearer that it is not just the saturated fatty acids that are the problem but the source or the food matrix of the saturated fatty acids and the foods that the saturated fatty acids are combined with. What do I mean by this? I am talking about the combination of refined carbohydrates with saturated fatty acids in food items such as deep-fried foods and store-bought baked goods.
I learnt that excess carbohydrates can have some very nasty effects on the human body, such as increasing liver fat stores resulting in small, dense LDL (sd-LDL) particles (23) (when it comes to lipoproteins and cardiovascular health, the bigger the better!) So what does this mean? Both saturated fatty acids AND excess carbohydrates result in an increase in LDL particles in the circulation and in fact, the increase in LDLs caused by excess carbohydrates is worse (31, 32)! Carbohydrates from the diet appear to increase circulating saturated fatty acids more than dietary saturated fatty acids themselves (33-36)! I found this information quite shocking but when you think about it, it makes sense considering what the typical Western diet is composed of. Hence why I am always going on about ‘no refined carbohydrates’.
OK, so it seems that saturated fatty acids are not as terrible as scientists once believed and that excess carbohydrates are the real bad guys when it comes to cardiovascular health. But I seem to be getting side tracked. I am supposed to be discussing whether nuts are healthy for your heart. Let me summarize my thoughts so far. In many of the studies in which nuts were substituted for other components of the diet, I believe, and so do researchers in this field, that it was the elimination of certain foods, namely saturated fats and refined carbohydrates, that led to the improved cardiovascular outcomes. So is there any evidence suggesting that adding nuts to the diet could lead to beneficial blood lipid and lipoprotein changes?
MUFAs and cardiovascular health
Let’s start with the MUFAs found in nuts. I can find little evidence for any mechanisms by which oleic acid, the main MUFA in nuts, improves cardiovascular risk factors. The only improvements occur when this MUFA is used to replace SFAs (37), but again we have to be aware of what these SFAs are combined with ie. refined carbohydrates. In contrast, a pooled analysis of 11 cohort studies reported that the replacement of SFA with MUFA was not associated with a decreased risk of coronary heart disease death or events (38).
Although the Mediterranean diet, which includes extra virgin olive oil and nuts, both sources of oleic acid, is associated with reduced cardiovascular disease, it seems that it is the combination of foods and nutrients in this diet, and not the oleic acid itself, that is responsible for these positive effects (39). I also came across a rather interesting recently published review, which looks at the food processing methods in the Mediterranean diet. The Mediterranean diet includes the consumption of raw cruciferous vegetables, such as rocket (arugula) in salads and wild greens, raw onions and garlic, stewed rather than boiled vegetables, raw extra virgin olive oil, raw nuts with the skins on and meats marinated in low pH substances such as lemon juice and vinegar. These methods of food preparation may enhance and retain the nutritional quality of the food and may contribute to the health benefits associated with the Mediterranean diet (40). I also believe that the consumption of unrefined, unprocessed foods provides greater feelings of satiety and prevents overeating.
The only positive impact of oleic acid I came across was that compared to omega-6 (or n-6) PUFAs, such as linoleic acid, it renders LDL fairly resistant to oxidation (41-43). How would this contribute to cardiovascular health? Well atherosclerosis is caused by chronic inflammation affecting large and medium sized arteries. This inflammation is initiated by a build up and oxidation of LDL particles in the artery wall leading to the formation of plaques (44). Therefore, reducing the oxidation of LDL can reduce the potential for plaque formation.
The other MUFA found in nuts is palmitoleic acid, however, it is only macadamia nuts that are particularly rich in this fatty acid. Several studies have shown an improvement in blood lipids and lipoprotein profiles with the incorporation of macadamia nuts into the diet (45-47). The subjects in these studies were mostly hypercholesterolemic and were consuming a ‘typical American diet’ so we cannot rule out the possibility that it was the elimination of particular foods rather than the incorporation of the macadamia nuts that was responsible for the results observed. I keep repeating this statement but it is something that you must be aware of when interpreting results from these ‘startling’ or ‘alarming’ nutritional science studies.
One study I found looked at the impact of specific fatty acids on the cardiovascular health of hamsters. Groups of hamsters were fed diets enriched in macadamia oil, canola oil (containing oleic acid), safflower oil (containing the n-6 PUFA linoleic acid) or a combination of palm and coconut oil (both containing SFAs) (48). I know hamsters are not people but it turns out that hamsters have similar cholesterol and bile acid metabolism and responsiveness to changes in dietary fatty acids and cholesterol as humans (49-52). After 18 weeks of feeding (poor hamsters!), the study found that those groups of hamsters feed macadamia, canola and safflower oil-enriched diets had similar non-HDL cholesterol concentrations. These concentrations were all lower than those hamsters fed the palm/coconut oil-enriched diet. Plasma HDL-C concentrations were higher in the macadamia nut oil-fed hamsters compared with the 3 other diet groups. Low non-HDL cholesterol and high HDL-C are both positive outcomes for cardiovascular health. This shows that oils rich in MUFAs and PUFAs have a less atherogenic plasma lipoprotein profile compared to oils rich in SFAs when other components of the diet are kept consistent, at least in hamsters anyway. But be aware that these hamsters were being feed 10% of their total diet as the test oil, which seems like a lot of oil to me. Also, the total carbohydrate content of the hamster’s diet was 50%. I thought this was quite high, and may be a contributing factor to the effects of the SFAs on non HDL-C levels.
The proposed mechanism responsible for the cholesterol lowering effects of dietary MUFAs or PUFAs is believed to be the upregulation or increase in hepatic (liver) LDL receptor activity, which promotes clearance of circulating LDL. On the other hand, dietary SFA reduce this effect by suppressing hepatic LDL receptor activity, as I mentioned earlier. Basically the LDL receptor, which is found mainly on the surface of liver cells, is responsible for binding LDL-C and removing it from the circulation.
Despite this proposed mechanism, when we look at large cohort studies assessing the association between MUFAs and CVD risk, there is no evidence that consumption of MUFAs reduces the risk for CVD (53, 54).
There is an issue that has been brought to my attention since I have started reading more in the field of nutritional science. A large cohort study will be published claiming that a particular food component is ASSOCIATED with a disease, for example, SFAs with CVD. However, when scientists in the lab try to figure out the mechanisms to explain this association, the data is often conflicting or does not support the association. This is because food contains an array of nutrients; polyphenols, antioxidants, vitamins, minerals, etc. and this mixture of nutrients and the cumulative effect that they have on the human body in the context of the rest of the diet, is very difficult to assess. Plus we are all unique individuals with a unique genetic makeup, which we are only now starting to decipher thanks to the advances in DNA sequencing technology. Also, the other issue I am finding with the field of nutritional science is that it is virtually impossible to conduct long-term, controlled studies on people (bacteria are much better for this because their life span can be over in as little as 20 minutes). This makes it very difficult to assess the full impact of a particular food component to human health and disease.
Now back to dietary fats.
n-6 PUFAs and cardiovascular health
Linoleic acid (LA), an essential fatty acid produced in plants, is the main n-6 PUFA in the human diet.
In human cells LA has been shown to increase LDL receptor gene and protein expression and reduce cholesterol production by binding to the DNA regulatory proteins known as the sterol response element binding proteins (SREBPs) (55), both of which would be considered positive impacts on cardiovascular health. However, increasing LA content in LDL enhances its ability to become oxidized, which is potentially proatherogenic (56). These results seem conflicting.
While we are on the topic of n-6 PUFAs, I will discuss the importance of the ratio between n-6 and n-3 PUFAs. Due to the association that was made between SFAs and CVD in the second half of the 20th century (although it is becoming clear that this claim was not entirely valid) there was a shift in Western countries to replace butter and animal fats with vegetable oils rich in n-6 PUFAs. The research now shows that the balance of n-6 to n-3 PUFAs may be problematic. Excessive amounts of n-6 fatty acids, which are mostly found in vegetable oils, relative to n-3 fatty acids have been associated with detrimental impacts on health including the worsening of conditions such as atherosclerosis, arthritis, asthma, bone loss, cancer growth, heart attacks, depression, suicide and length of hospital stay (57-59). This may be due to the competition between the n-6 PUFA LA and the n-3 PUFA ALA for the same enzymes during their conversion to the eicosanoids: thromboxanes, leukotrienes and prostacyclin. Eicosanoids are signalling lipids. High dietary intakes of LA block the metabolism of ALA, resulting in the formation of the pro-thrombotic (promoting blood clotting) and pro-inflammatory eicosanoids thromboxanes and leukotrienes. It has been reported that the ratio of n-6 PUFA to n-3 PUFA ranges from 2:1 to 1:1 in the traditional Mediterranean diet compared to 15:1 in the European diet and about 17:1 in the Northern American diet (60). I don’t mean to scare you but this is something to consider for your long-term health. I would be keeping an eye on the amount of vegetable oils or n-6 PUFAs in your diet. These are often used in heavily processed and packaged foods.
n-3 PUFAs and cardiovascular health
There is evidence that the n-3 or omega-3 PUFAs from marine sources, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have unique cardioprotective properties. These fatty acids appear to suppress inflammatory responses that are critical to the initiation of atherosclerosis (61-64). Also, supplementary EPA and DHA has been shown to incorporate into the plasma membrane (65) and the mitochondria (66) of normal growing cells. Specifically, supplemented EPA and DHA can incorporate into the phospholipid cardiolipin. Cardiolipin plays an important role in maintaining heart metabolism, cellular respiration and mitochondrial function. This may explain the mechanisms accounting for the protective properties of EPA and DHA (67). Whether the plant-derived n-3 PUFA α-linolenic acid (ALA) has similar properties is not conclusive although there are an increasing number of studies supporting the cardioprotective benefits of ALA (68).
Walnuts are the only nuts that contain the short chain n-3 PUFA ALA. ALA is converted to the longer chain n-3 fatty acids EPA and DHA, however, the conversion efficiency is very low. Only 5% of ALA is converted to EPA while less than 1% is converted to DHA (69). Due to this low conversion rate, it seems that ALA has health benefits that are unrelated to its role as a precursor to the long-chain n-3 PUFAs. Evidence from prospective studies suggests a modest protective effect of ALA consumption on CVD outcomes (70), however, random clinical trials showing a causal relationship are lacking. In 2014, 3 random clinical trials had been conducted assessing the impact of ALA on CVD risk reduction (71-73). Overall, these random clinical trials showed reductions in CVD risk due to the consumption of ALA, but some flaws were identified in these studies. For example, in one study dietary components other than ALA were changed and in another study the subjects were not blinded to the treatments (68).
Endothelial dysfunction is a crucial event in atherogenesis: the formation of abnormal fatty or lipid masses in arterial walls. Atherogenesis can lead to atherosclerosis, which is the major cause of CVD (74). Numerous studies have shown that diets enriched with walnuts can reduce markers of endothelial dysfunction, both in the short-term and long-term (75-81). It should be noted that these studies were conducted on hypercholesterolemic subjects or subjects at high cardiovascular risk, and not healthy subjects. The ALA in walnuts may play a role in improving endothelial function. A study published in 2014 in the British Journal of Nutrition entitled ‘Effects of an energy-restricted diet rich in plant-derived α-linolenic acid on systemic inflammation and endothelial function in overweight-to-obese patients with metabolic syndrome traits’ included 95 patients that were randomly assigned to either an energy-restricted diet enriched with ALA (3.4 grams ALA/day) or an energy-restricted control diet (approximately 0.9 grams ALA/day) for 26 weeks. The consumption of fish, fish oil capsules and foods enriched with n-3 fatty acids were not allowed. Many parameters of the patients were measured after the 26-week dietary intervention including body composition, serum lipid concentrations, insulin, glucose, blood pressure and biomarkers of endothelial function and inflammation in the fasted state. After the 26-week intervention period there was clear improvements in biomarkers of endothelial function, resting blood pressure and inflammation in both the ALA enriched group and the control group. These improvements were likely attributed to the loss in body fat experienced by the patients in both groups. This highlights the importance of maintaining a healthy weight range. The only differences between the ALA enriched diet group and the control group were that the ALA group showed greater reductions in diastolic blood pressure and in serum YKL-40 concentration. YKL-40 is a glycoprotein that is a potent angiogenic factor (82), meaning it promotes the growth of new blood vessels, and is thought to facilitate the formation of atherosclerotic plaques (83). Elevated serum levels of YKL-40 have been found in patients with CVD (84, 85). These results indicate that ALA may have some positive impacts on CVD risk factors in overweight and obese patients. There is also evidence that ALA has anti-inflammatory effects (86-88), however, more research is needed to confirm these findings.
One study found that a walnut-enriched diet increased the clearance of LDL-C in human liver cells. This clearance was increased as amounts of ALA increased in the LDL particle suggesting that ALA may play a role in decreasing LDL-C concentrations (89).
Other beneficial compounds in nuts
As well as being a rich source of unsaturated fatty acids, nuts are a good source of protein, with a high content of the amino acid L-arginine. L-arginine is used to make endothelium-derived nitric oxide (NO). NO is the main regulator of vascular tone and blood pressure (90). This may contribute to the positive effects on vascular reactivity that have also been reported for diets containing nuts.
Nuts are a rich source of a variety of vitamins and minerals, including tocopherols, folate, magnesium, zinc and calcium (91). Additionally, nuts are abundant in the antioxidant compounds polyphenols. In fact raw walnuts provide the 7th largest amount of total polyphenols among common foods and beverages tested. Polyphenols extracted from various nuts have the ability to inhibit the oxidation of LDL and VLDL, with walnuts being the most efficacious (92). Human studies have supported these findings showing that the oxidation of LDL is decreased following the consumption of pecans when compared to a test meal with an equivalent energy, macronutrient, and fluid content. The control meal was composed of refined olive oil, whey protein, white bread, and water (93). Decreases in serum oxidized LDL have also been observed in studies involving subjects consuming diets rich in walnuts (76, 77), almonds (94), hazelnuts (95), pistachios (96) and macadamia nuts (97). It also seems that the polyphenols in nuts enhance the antioxidant effects of other nutrients in nuts and other foods (98). Animal studies have also investigated the antioxidant nature of nuts. A 10-week study conducted in rats showed that consumption of pistachio nuts as 20% of the total daily caloric intake led to improvements, not only in HDL-C and in the total cholesterol/HDL-C ratio, but also inhibited LDL cholesterol oxidation. The researchers found that the activity of the antioxidant enzymes paraoxonase and arylesterase was increased significantly in the rats feed their 20% daily caloric intakes as pistachios. These enzymes are both known to protect LDL from oxidation. However, the researchers found that the activity of these potentially beneficial enzymes were not further increased in rats feed 40% of their total daily caloric intake as pistachios (99). This suggests that more is not necessarily better and that the other components in nuts apart from the fats may have beneficial cardiovascular effects.
Another more simple explanation for the potential cardiovascular health benefits associated with nut consumption is the satiety effect. In other words, nuts make you feel full because they are so dense in calories due to the high content of unsaturated fatty acids. Raw nuts are also high in fibre. Regular consumers of nuts may be less tempted to over eat foods that are more detrimental to cardiovascular health, such as refined carbohydrates and trans fatty acids.
Nuts and weight loss
While there is no epidemiological or clinical trial evidence showing that frequent nut consumption promotes weight gain (3), let’s not forget that nuts are very energy dense meaning they are very high in calories. Although nuts appear to have health benefits when included in a calorie controlled diet, the excess consumption of nuts is not conducive to weight loss. The main issue with nuts is that they are very easy to over consume. They are crunchy and tasty and you tell yourself ‘It’s OK – they are healthy’ and the next thing you know you have eaten a whole bag of pistachios! From my own personal experience, if I am trying to lose weight, I will reduce my nut intake to 10, at the most 15 nuts per day and eliminate nut butters. I thoroughly enjoy nuts and nut butters as they are delicious and low in carbohydrates, but if I feel that my weight is creeping up, nuts are one of the first food items I will reduce. So if you are in the process of trying to lose weight, I would leave nuts off the menu until you achieve your goal weight. If you are overweight, the best way to improve CVD risk factors is to lose weight (32, 100).
Is the consumption of nuts beneficial for healthy people?
It seems to me that in the majority of the studies conducted looking at the impacts of nut consumption on blood lipid profiles, the subjects are eating a ‘typical American diet’. This diet is pretty awful and consists of refined carbohydrates, processed meats, unfermented dairy and minimal vegetables. Furthermore, the subjects in most studies have elevated cholesterol levels to begin with. I was interested to find out if nuts have any cardiovascular benefits for healthy people who are within an ideal weight range? The most recent and comprehensive review that I came across was published in September 2015 and was entitled ‘Nut consumption for the primary prevention of cardiovascular disease’. The aim of this review was to answer the question whether or not increasing the consumption of nuts can prevent CVD in healthy adults or adults at risk of CVD. The conclusions of this review were that there is no evidence for the effects of nut consumption on CVD clinical events in primary prevention and that there is insufficient evidence to indicate that increased nut consumption will reduce the risk of CVD in healthy individuals (101).
Conclusion: Replacing saturated fats and refined carbohydrates with nuts may be beneficial for people at risk for CVD but not necessarily for already healthy people
Cardiovascular disease (CVD) is ranked as the top global health problem and nutrition affects many CVD risk factors. Therefore, it is important to consider the impact the foods you eat have on your cardiovascular health. Back in the early 1980’s the recommendation to reduce the risk of CVD was to replace SFAs with dietary carbohydrates, however, this information was not based on solid scientific data. More recently there has been recommendations to replace SFA with unsaturated fatty acids, including those found in nuts. For people who are at risk for CVD replacing some components of the diet, such as refined carbohydrates and foods high in saturated fats with a small serving of nuts may be beneficial for cardiovascular health.
In healthy people I believe that there is insufficient evidence to conclude that the consumption of nuts reduces the risk of CVD. However, the recommendation made by the 2010 Dietary Guidelines Advisory Committee to Americans stated: “There is moderate evidence that consumption of unsalted peanuts and tree nuts, specifically walnuts, almonds, and pistachios, in the context of a nutritionally adequate diet and when total calorie intake is held constant, has a favorable impact on cardiovascular disease risk factors, particularly serum lipid level” (102). Nuts do contain a range of other potentially beneficial compounds and a small serving (by small I mean 50 grams) most days of the week can contribute to a healthy diet. I personally define a healthy diet as one that is rich in vegetables and lean sources of protein containing some dairy, particularly fermented dairy, quality fats ie. mostly plant and marine n-3 PUFAs with some SFAs (remember that too many n-6 PUFAs relative to n-3 PUFAs can be detrimental to health), with limited refined carbohydrates and is virtually without industrial trans fatty acids. The research unequivocally shows that trans fatty acids increase LDL-C and decrease HDL-C (103). Most importantly a healthy diet should not exceed the daily calorie requirements of the individual. As with most things in life, moderation is the key and avoid anything in excess. Finally, don’t be fooled into thinking that nuts are completely healthy and that you can eat as many as you like – remember anything in excess is not good for you.
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