There is no one “MS diet,” just as there is no one universal MS experience. Some of the diets intended for use in MS have a few features in common – for example, they nearly all advise to eliminate ultra-processed foods – but they can also have considerable differences. The goal of these diets is to adequately nourish, eliminate toxic and otherwise aggravating influences, and exert anti-inflammatory, antioxidant, and remyelination benefits 142.
MS diets frequently feature avoidance of ultraprocessed foods. While most foods are processed in some way – even rinsing of produce prior to sale is considered processing – there are degrees (Harvard University, undated-a), and they make for key differences in effects on the body.
Ultraprocessed food and artificial food additive consumption is rising globally143-147, concurrently with the incidence of autoimmune diseases 148,149, including that of MS 9,149. Ultraprocessed food intake may impact disease risk by contributing to obesity and through exposure to food additives and contaminants 143, and has been associated with increased systemic inflammation 150.
Ultraprocessed foods tend to be of a poorer nutritional quality than minimally processed foods 151-156. Diets high in ultraprocessed foods have been observed to have greater energy density (more calories per weight), free sugar, and overall, saturated, and trans fats, and to be lower in fiber, protein, and essential minerals 151,153-155. As may be expected, individuals who follow such a diet tend to eat more calories (mainly from simple carbohydrates and fats) and gain more weight when compared to consumers of unprocessed diets 157, and are more prone to obesity 156,158-165, a suspected risk factor for MS 112,166.
Common food additives have been shown to negatively affect the intestinal epithelial barrier, which serves to protect the body from immune-triggering foreign agents. A compromised barrier and its “tight junction” have been linked to intestinal permeability – otherwise known as “leaky gut” – and ultimately to development of autoimmune disease. Tight junction leakage is particularly worsened by refined sugar 167-171, salt, certain emulsifiers, organic solvents, gluten, microbial transglutaminase, and nanoparticles, all of which are extensively and increasingly used by the food industry “to improve the qualities of food.” These additives may contribute to barrier dysfunction and ultimately permeability, resulting in entry of harmful antigens and activation of the autoimmune cascade 172.
Food contaminants, such as chemicals that are newly formed during the processing itself, have also been suggested as potential mechanisms linking ultraprocessed foods to higher disease risk. Through the associated chemical and biological transformations, the fundamental structure of the food changes, inducing the creation of “neoformed” substances like trans-fat, acrylamide, heterocyclic amines, polycyclic aromatic hydrocarbons, oxyhalides, and haloacetic acids, some of which are considered neurotoxic173,174. Additionally, some contaminants from food packaging, such as bisphenol A (BPA) have been observed to exert endocrine (hormonal)-disrupting effects 175 that may translate to autoimmune dysfunction 176 and neurogenerative disease 177, including MS 178.
Another potentially problematic component of processed foods is salt, specifically the sodium types. While sodium is an essential nutrient that contributes to the body’s normal functions – including neuromuscular – excessive intake has been associated with certain health risks in the cardiovascular system and kidneys. Salt is not often given specific attention in MS diets, but has been addressed in the scientific literature in the context of autoimmune disease, including MS, where findings are mostly of salt’s harm at excessive levels, e.g., more than 5 grams per day 179-181, though some animal studies have observed benefit 182,183.
Certain regulatory immune cells called Tregs are critical for “self-tolerance” (which keeps the body from attacking itself) and can be defective in autoimmunity. In MS, dysfunctional self-tolerance is partially enabled by dysfunctional Tregs that secrete interferon-gamma (IFNγ). It has been shown that increasing salt significantly impairs Treg function by increasing their IFNγ secretion, thus promoting proinflammatory autoimmune responses 184.
Additionally, it has been observed that high intake of salt (e.g., equivalent to 5400 mg/day of sodium) may contribute to CNS autoimmunity by promoting neuroinflammation-driving immune cell (Th17) responses 179,180 and changes in microbiota in both animals and healthy humans 185, linked specifically to worsening rather than initiation of disease 186,187. Fortunately, the reduction in friendly bacteria and associated immune cell reaction may be reversible with probiotic supplementation 185.
Among MS patients, a small study found sodium intake above 2000 mg/day to be associated with approximately three-fold increased exacerbation rate and radiological disease activity (including total T2 and CUA lesions) 188. Later and larger clinical studies found no such association 189, including in children 190,191. No less important, however, it was demonstrated that the effects of dietary sodium on autoimmune neuroinflammation are dependent upon genetics and gender, tending to impact females more 192.
Interestingly, it was shown in an animal study that high salt intake could curtail development of autoimmune disease. It may do this this by promoting tightening of the blood-brain barrier, thereby limiting entry of inflammatory T-cells into the CNS. The extra consumption of sodium 183,193,194 was equivalent to approximately 1350 mg in the average modern western human diet 95, which would bring the total to about 3750 mg, in line with average global intake 196-198 – 60% more than the 2300 mg daily recommended in the United States based on cardiovascular research 199, but less than the 5000 mg upper limit recommended by the World Health Organization (WHO)200.
The bottom line appears to be that salt restriction below national and international recommendations should perhaps be sought in women with active autoimmune disease and genetic predisposition to salt-sensitivity, with good probiotic intake among higher sodium consumers.
A major difference between popular MS programs is the amount of fat recommended, ranging from the lowest in the Swank and McDougall diets to the highest in the ketogenic plan. The following is some background regarding the effects of fat on the body and what foods are the highest sources.
The brain is high in fats, which support structural, biochemical and cell signaling functions 201,202. Local “cerebral” changes in fat balance have been associated with neurodegenerative disorders 203-206.
The fats involved in brain and other bodily functions need to be obtained from food or synthesized from building blocks in food. The brain typically gets its energy from sugar, made from carbohydrate and protein, but evolutionarily may have run on products of fats called ketones, something that is increasingly explored today 201.
The components of food that provide energy (calories) are fat, protein, carbohydrate, and alcohol. Of these, fat is the most dense, providing 9 calories per gram, compared to 7 in alcohol, 4 in protein, 4 in carbohydrate, and up to 2 in soluble fiber (a type of carbohydrate).
Fat is constructed by a glycerol “backbone” supporting fatty acids. There are two main types of fatty acids, saturated and unsaturated, with the latter further categorized into monounsaturated and polyunsaturated. Foods generally contain a combination of fatty acids from each of the categories, with differing proportions 201.
There is controversy about the association between total and different dietary fatty acids and risk of chronic “lifestyle” disorders such as coronary heart disease, an association that is considered to be relevant to MS.
Saturated Fatty Acids
These are highest in animal fat and hydrogenated, coconut, and palm oils. Saturated fats are completely solid at room or colder temperatures but liquefy in heat.
The long-term studies conducted by Roy Swank showed a close connection between saturated fat intake and the development and progression of MS. Specifically, it was found that MS patients who avoided saturated fats and favored unsaturated fats typically had reduced progression of MS 207. High levels of saturated fats have also been linked to cardiovascular disease and obesity 208,209 and are regularly used in experimental models to induce metabolic disruption 209,210. They may cause immune stimulation and inflammation 211, which can worsen MS symptoms.
A 2021 study of nearly 386,000 patients in nine countries found associations of saturated fatty acids with coronary heart disease in opposite directions depending on the food source: disease incidence was lower with greater intake of saturated fats from yogurt, cheese, and fish, but higher with saturated fats from red meat and butter 212.
Monounsaturated Fatty Acids
These are most commonly associated with plant foods such as avocado and its oil, certain nuts (including macadamia and hazelnut) and their oils, modified seeds (high-oleic sunflower and safflower) and their oils, and olive and its oil. Monounsaturates are also high in meats, particularly beef and pork, as well as high-fat hard cheeses such as cheddar, though the specific fatty acid make-up tends to be different from that in plant foods, with different effects on the body 213. Monounsaturated fats are liquid at room and warmer temperatures but solidify somewhat when refrigerated.
Monounsaturated fatty acids tend to be less associated with a high-risk cardiovascular profile than saturated fatty acids, and in some studies have been associated with significant health benefits, such as prevention of the metabolic syndrome and its complications 214.
Polyunsaturated Fatty Acids
Rich plant sources are primarily nuts and seeds and their oils, including flaxseed (linseed), grapeseed, pumpkin seed, rapeseed (canola), regular sunflower and safflower seed, sesame seed, almonds, peanuts, and walnuts; additional vegetal sources are corn, rice bran, and soybean and their oils. Rich animal sources include fatty fish such as mackerel, salmon, sardine, swordfish, trout, and tuna, as well as eggs. Polyunsaturated fats are liquid at all temperatures, and are prone to oxidation 215, more so than saturated fats 216.
Polyunsaturated fatty acids are commonly categorized into omega-3 and omega-6 varieties. Only these two groups are essential in the human diet (meaning we need to get them from food) and have their respective roles in the body 217. Both are involved in neurological function 218.
Unfortunately, modern western diets high in processed foods often provide a disproportionately high amount of omega-6s 219, which can be pro-inflammatory, and not enough omega-3s, which tend to be anti-inflammatory. Of note, traditional diets of populations with long healthy lives provide ratios between omega-6 to omega-3 of 5:1 or lower, compared to over 15:1 in the United States 220.
Polyunsaturated fats have long been recommended as a substitute for saturated fats in the diet to prevent and/or manage cardiovascular disease risk factors 221 and related health issues such as non-alcoholic fatty liver disease 214.
Hydrogenated Fats
Because polyunsaturated fats are highly susceptible to spoilage and often behave differently in food preparation than do saturated/hard fats, they may be “hydrogenated” to be hard at room temperature and resistant to rancidity and oxidization. The process, called “hydrogenation,” can extend the shelf life of products and mimic the structural properties and mouthfeel of saturated fat. Unfortunately, hydrogenation leads to generation of artificial trans-fatty acids, which have been linked to harmful processes in the body, including cancer, heart disease, and immune dysfunction 222.
Rules for Oil Use and Storage:
Carbohydrates are the main source of energy (calories) in most food patterns around the world, with some cultures taking in up to 70% of their energy from that source. In contrast, some cultures have long survived on diets higher in fat and protein. In the modern western world, people are increasingly interested in reducing their carbohydrate intake for health reasons. Diets promoted for MS management range widely in their carbohydrate content, from the very high McDougall to the very low ketogenic and carnivore.
When the most basic carbohydrate – the simple sugar glucose – is available in the body, the human brain uses about 25% of the total for energy production, with the highest energy requirement in adult brain cells (neurons) 223. It was long thought that a continuous supply of glucose is needed from the bloodstream to the brain, as with a few exceptions, glucose has been considered to be the main source of energy 224. However, the brain can also use ketone bodies as an energy source, as observed in starvation, during strenuous exercise and development 225, and of course, when following a ketogenic diet. Whatever the predominant energy source, tight regulation of its metabolism is necessary for normal brain function, and any disturbances may contribute to the pathology of brain disorders 226.
Studies show that energy metabolism in the CNS of MS patients may be abnormal 227. Increased activity of metabolic enzymes in the cerebrospinal fluid of patients with disseminated sclerosis make them a sensitive indicator of active demyelination. The observed alterations in energy metabolism may contribute to the mitochondrial dysfunction and nerve fiber degeneration underlying MS progression 228. In demyelinating diseases, particularly MS, it is likely that cells need ample energy to survive. Unfortunately, the mechanism of energy-generating molecules in MS lesions may be reduced 229.
Significantly reduced “insulin sensitivity” (also called “insulin resistance”) has been observed in MS patients compared to healthy comparators (also known as “controls”) 230-233, and has frequently been linked to MS 234. Insulin is a hormone in the body that functions to pull glucose from the bloodstream into cells, including neurons, for use. Sensitivity to insulin is important not only for healthy energy production, but also to prevent glucose and insulin itself from building up in the bloodstream and causing neuronal dysfunction and even damage 235,236. Too much insulin in the blood (a condition known as “hyperinsulinemia”) has been linked to neurodegenerative disorders 236, including MS 237. One study found insulin resistance and impaired glucose metabolism already at an early stage of MS 230. No less importantly, other studies showed a link between the degree of insulin resistance in MS patients and severity of disability 233, chronic inflammation, and oxidative stress 231.
The principal food component associated with conversion to glucose and need for insulin activity in the body is carbohydrate. The type of carbohydrate that converts most rapidly is known as “simple,” and is highest in white sugar, associated foods such as syrups and candies, and refined grain and grain-substitute products, such as potato and tapioca flours. Fruits can also be high in simple carbohydrates, but they also contain complex carbohydrates – notably fiber – and water, which slow the conversion process. While most simple carbohydrate foods and beverages have been associated with impaired metabolism and inflammation, complex carbohydrate foods high in fiber have been attributed protective metabolic effects, including on brain function 238.
Numerous studies have compared the respective benefits of high-carbohydrate versus low-carbohydrate diets on health parameters such as weight management and control of blood glucose levels, with conflicting results. Recent data suggest that a well-composed high-carbohydrate diet can have a metabolic influence similar to that of a low-carbohydrate diet, well-composed meaning high in fiber and low in refined carbohydrates and glycemic index (GI) 239,240. GI is a scoring system of carbohydrate-rich foods according to how much each increases blood sugar levels 241, and while its adequacy has been debated, it is used as a general basis for assessing carbohydrate food quality.
MS diets range from vegan to meat-rich Paleo in their animal product content, each with their specific justifications. Of the animal foods, dairy is the most commonly omitted, followed by eggs. As with other sensitivity issues, different bodies respond differently to different approaches, and each diet has their own advantages and disadvantages.
A vegan approach, as promoted by Dr.s John McDougall and Saray Stancic, omits all animal foods, and some people have found success in managing their MS with such plans. One of the reasons may be the lack of potentially aggravating factors found in meat 242, dairy243-245, and eggs 244-246, while another may be the particularly high content of powerful antioxidants and important fiber in plant foods247. Like most diets that omit major food groups, it is important to make sure your plan provides adequate nutrition and is not based on refined or ultraprocessed foods. Additionally, you should listen to your body and take care to not replace one set of allergenic or inflammatory factors with another. Common causes of controversy include legumes, given their lectin content, gluten, which is considered to be inflammatory even in non-celiac individuals, and grains in general, due also to lectins. These are discussed below.
The meat-inclusive Paleo approach favored by Dr.s Terry Wahls, Loren Cordain, and Sarah Ballantyne has also met with success in MS cases. It owes its influence in large part due to the omission of overly processed foods, but according to Wahls, also triggering foods such plant-based sources of protein (primarily legumes), eggs, and dairy.
Eating more meat, having less of certain bacteria in the gut, and more of certain immune cells in the blood, all link with MS. A recent analysis demonstrated an association between greater meat consumption and a decrease in the commensal (or helpful) species Bacteroides thetaiotaomicron in the intestines. This bacteria has been found to be protective against autoimmune disease 248, and is involved in digesting carbohydrates from vegetables, which in turn serve to feed other commensals that are important for general health 249. Higher meat consumption in MS patients was also linked to increased harmful Th17 cells in the immune system 242. While some healthy people eat a lot of meat, the analysis suggested that in MS, gut bacteria is disconnected from proper immune function, leading to greater autoimmune attacks on the nervous system with meat consumption 242. It is important to note that since the analysis was performed on widely differing populations, the quality of the meat may have been inferior to the pastured and grass-fed types recommended in some MS diets.
Eggs are a potential allergen246, the second most common food allergy in the United States after dairy, affecting primarily children 250. In adults, eggs are associated with possibly greater allergenicity in inflammatory autoimmune disorders due to overactivated intestinal immunity 244. An animal model and survey in adults suggested that eggs may be associated with aggravation of autoimmune inflammation245. However, if allergy to eggs is not an issue, they can represent an important source of high-quality protein, vitamins, and minerals, and in the case of certain fortified types, anti-inflammatory omega-3 fatty acids, including the docosahexaenoic acid (DHA) sought in fatty fish 251-253.
Similarly to eggs, dairy is a common allergen that affects primarily children, but can also affect adults. Also similarly, dairy has been observed to aggravate autoimmune inflammation244,245, but more specifically, has been shown to correlate with MS prevalence 254. Dairy contains the protein butyrophilin, which mimics part of myelin oligodendrocyte glycoprotein (MOG) 243, believed to be important in the myelination of nerves 255 and to serve as a mediator of interactions between myelin and the immune system 256. Therefore, a sensitivity to dairy may result in the immune system targeting MOG, triggering an immune reaction central to MS243,257,258. Casein is another key protein in dairy, considered to be perhaps the most allergenic 259, and which may also have cross-sensitivity with MOG. There is evidence of how an immune response against casein can aggravate the demyelinating pathology of MS as a result of similarity to MOG 254. While these reactions are dependent upon there being a sensitivity to the proteins in dairy, potentially greater general food sensitivity in MS is a concern 260. If the inclusion of dairy products is desired, there are lower-risk options such as goat’s milk, whose protein composition favors whey over casein, and which studies have shown is very low in the troublesome alpha S1 type of casein and primarily contains alpha S2 casein, which is far less allergenic 261. Another option growing in popularity is A2 milk, free of the A1 variant of β-casein, a protein that represents approximately 30% of the caseins in cow’s milk. A2 releases much smaller amounts than A1 of bioactive opioid peptide β-casomorphin 7 upon digestion, linked to harmful effects on human health 262.
Nightshades are plants from the Solanaceae family, comprising fruits, vegetables, herbs, flower, and trees. Some are highly toxic to humans, whereas others are considered edible. Some of the most common among the edibles are listed below.
Ashwagandha
Eggplant
Goji Berries
Okra
Paprika
Peppers (vegetables and spices, such as cayenne)
Potatoes (white)
Tomatillos
Tomatoes
What create toxicity in nightshades are compounds called alkaloids, present in large amounts in poisonous members of this family, and in small amounts in the edible members. The latter are harmless to most people, especially when eaten fully ripe. Importantly, the majority of alkaloids are found in the stems and leaves, which are not normally eaten. In sensitive individuals, however, even a small amount of the alkaloids that can contribute to flares of autoimmune conditions such as MS. Saponins, another type of molecule in nightshades, can create the type of exaggerated response from the immune system observed in autoimmune disorders.
Many dietary approaches to MS include elimination of gluten and grains, while a few do not. This appears to be an individual issue, as some people thrive with grain intake, while others are more susceptible to the negative effects.
Observational studies have linked consumption of whole grain products with reduced risks for chronic inflammatory disorders such as type 2 diabetes, cardiovascular diseases, obesity, and some types of cancer 263, as well as decreased inflammatory markers (CRP, Il-6) 264. However, interventional studies do not always demonstrate a clear benefit265-270, and it has been speculated that other components in the diet or overall lifestyle may be impacting the immune response 271. For example, a diet high in whole grains with low glycemic index was associated with sustained reductions in glucose and inflammation in type 2 diabetics compared to a diet high in refined grain products with a high glycemic index. In addition to the inflammatory potential of glycemic index, whole grains contain phytochemicals that can exert anti-inflammatory effects, possibly offsetting potentially pro-inflammatory effects of gluten and other protein compounds called lectins 272. Of note, many intervention studies evaluating increased whole grain intake used refined grain diets as controls, thereby making it difficult to draw conclusions on the independent role of whole grains in disease and inflammation 273.
Wheat products have been reported to trigger allergic reactions such as rhinitis and asthma 274,275, which are essentially autoimmune in nature. Several proteins present in wheat, most notably gluten proteins, have been shown to react with an immune compound known as immunoglobulan E (IgE) in the body that is responsible for allergic responses 275.
More common than wheat allergies is gluten intolerance, which features in celiac disease, an autoimmune condition estimated to affect approximately 0.7-1.4% of the global population 276. Further, incidence of celiac disease is closely related to that of other autoimmune disorders such as type 1 diabetes, raising the possibility of a connection through gluten277,278.
Gluten is the main structural protein complex in wheat, making up about 80% of the total protein. It consists of glutenins and prolamins 279, the latter known as gliadins in wheat. Glutenins are polymers of individual proteins, while gliadins are monomeric proteins, classified as alpha/beta-gliadins, gamma-gliadins, and omega-gliadins 275. Gliadin antigens from wheat gluten and related prolamins from other gluten-containing cereal grains, including rye and barley, can trigger celiac disease in genetically susceptible people. Of note, while key genes (HLA-DQ2, HLA-DQ8) are active in nearly all celiac sufferers 278, there is a group of HLA-DQ2/DQ8-inactive individuals with digestive symptoms that respond well to a gluten-free diet 280,281. This is because gliadin’s stimulation of pro-inflammatory immune cells is not limited to celiac disease 278,282,283.
Gliadin interacts with immune cells by passing through the intestinal barrier, which exists to protect the rest of the body from offending substances present in the intestines 284,285. Gliadin does this by increasing barrier permeability, which is an important early step in autoimmune reactions 282,286,287. Chronically increased intestinal permeability (or leaky gut syndrome) allows for the undesirable movement of both microbial and dietary antigens to the bloodstream and ultimately a disturbance in immune tolerance 288. This has been associated with autoimmune diseases, including MS 284.
Though gluten sensitivity may not be causally linked to MS in general (Hadjivassiliou et al., 2003), and the prevalence of antigliadin antibodies has been found to be the same in MS patients as in the general population – about 10% (Sanders et al., 2003) – there appears to be a subset of patients who react to gluten not with digestive symptoms, but with a movement irregularity known as “ataxia” that improves with a gluten-free diet 289.
A systematic review of prospective studies and surveys investigating use of a gluten-free diet in MS revealed inconsistent results: some studies showed benefit, some did not, and one even found food sources of gluten such as cereals and breads to be protective 290. This suggests that other factors may be at play, and that each person’s response may be unique.
Aside from gluten, there are protein compounds in wheat (including Kamut®, einkorn, spelt), other grains (e.g., rye, barley, oats), gluten-free pseudograins (e.g., quinoa, amaranth, buckwheat, teff), and similarly used foods (e.g., corn, rice) known as lectins, which have been shown in experimental models to stimulate pro-inflammatory immune cells. Lectins serve as defense mechanisms of those food plants against other plants and fungi, and are widely recognized as anti-nutrients, meaning that in high amounts (generally obtained from inadequate cooking) they can lead to poor absorption of nutrients and in some cases, food poisoning and/or organ damage 291. A key lectin is wheat germ agglutinin, which itself has been found to impair the integrity of the intestinal wall and increase permeability, allowing passage of small molecules, including other lectins 292 into the systemic circulation. The combination of wheat germ agglutinin and gliadin can result in an increase in microbial and dietary antigens interacting with cells of the immune system. Lectins have also been suggested to contribute to autoimmune disease by presenting errant immune system codes293 and stimulating white blood cells 294. Additionally, plant lectins such as those in grains and legumes have been shown to activate a key inflammatory network in the body to promote inflammation, mitochondrial damage, and related disorders 295, including MS296.
Fortunately, cooking, sprouting, or fermenting foods high in lectins can reduce the content to a negligible amount. No less importantly, a comprehensive review of the evidence from human trials has indicated that lectin-rich foods may not consistently cause inflammation, intestinal permeability, or nutrient absorption issues in the general population 297. However, there are clearly some individuals who respond unfavorably, and therefore may benefit from eliminating them 293.
For those who can safely consume them, lectin-rich plant foods are excellent sources of essential amino acids, prebiotic fibers, vitamins, minerals as well as powerful antioxidant and even anti-inflammatory compounds298,299, and are associated with reduced inflammatory biomarkers in both animal and human trials 300-303.
Legumes, including lentils, beans, peas, and peanuts, have long been an important source of protein, vitamins, minerals, and fiber in the food supply 304. Some legumes have attracted scientific attention because of their health-promoting effects, including prevention and management of chronic diseases such as cancers, cardiovascular disease, obesity, and diabetes 304,305. These have been attributed to antioxidant and anti-inflammatory properties from compounds such as phenolic acids, flavonols, flavones, isoflavones, anthocyanins, saponins, and tannins306-309.
Legumes are also high in lectins (read more about these in “Grains and Pseudograins”), and thus are sometimes omitted from autoimmune diets. Negative effects of raw legume lectins have been observed in animals. In the digestive system, these include decreased acid secretion and changes in the intestines that can lead to poor nutritional 310-315, and systemic effects include promotion of inflammation and altered immune function295,316.
However, just like grain sources, legume lectins can be minimized through cooking, sprouting, and fermenting291,297. Moreover, beneficial antioxidant and anti-inflammatory compounds can actually be increased in the process 300.
Of note, some legume lectins may themselves be beneficial, and in fact are being explored for their anti-cancer assistance – they can identify cancer cells, and therefore can improve the target specificity of conventional chemotherapy agents, potentially reducing harmful side effects317-319. Moreover, legume lectins isolated from lentils, chickpeas, jack beans, peas, and common beans have all demonstrated their own activity against various cancer cell lines320.
Since legumes are rich in nutrients, antioxidants, and anti-inflammatory compounds, it is recommended to only eliminate them after careful assessment of a genuine need321,322.
Nuts and seeds can induce an allergic reaction – a type of autoimmunity – in some people, and so may be eliminated to prevent triggering responses relevant to MS. In the Autoimmune Protocol (AIP) Diet, they are among the foods to be avoided during the initial phase, though they may be added back if tolerated.
As early as 1936, a link between food allergies and multiple sclerosis was suspected 323. Soon after, it was noted that the most severe MS attacks were in individuals with food allergies 324. It was more recently observed that people with autoimmune disease are more likely to have biochemically confirmed food intolerances than healthy people 260. In turn, MS patients with food allergies were shown to have more relapses and a higher likelihood of lesions compared with those with no known allergy257.
Peanut allergies are well-known, but tree nuts (e.g., almonds, Brazil nuts, cashew nuts, hazelnuts, macadamia nuts, pecans, pine nuts, pistachios, walnuts) can also elicit severe symptoms and a life-threatening anaphylactic reaction. Together with peanuts, hazelnuts account for 90% of deaths due to food allergy. Importantly, peanut – being a legume with characteristics of a nut – can cross-react with other plant-based foods, notably other legumes and tree nuts, meaning that peanut-allergic individuals can be both co-sensitized and co-allergic to such items. Unfortunately, desensitization to peanut – a form of oral immunotherapy to improve the body’s tolerance – has not been shown to have an effect on legume cross-sensitization325.
Allergies to seeds (e.g., coriander, mustard, poppy, pumpkin, sesame, sunflower) tend to be rarer, with sesame seed considered to be the most allergenic, affecting people of all ages 326.
For people who are not sensitive to their allergenic potential, nuts are valuable nutrient-dense foods rich in monounsaturated and polyunsaturated fatty acids and other bioactive compounds, including protein, fiber, minerals, tocopherols (vitamin E and related compounds), phytosterols, and antioxidant phenolics 327. Through these nutrients and phytochemicals, nuts have been linked to wide-ranging health benefits. Observational studies in humans report that nut consumption is associated with lower risks for cardiovascular disease, high blood pressure, cancer, and premature death. At the randomized clinical trial level, the PREDIMED study showed a protective effect of nuts against cardiovascular disease, and other human studies showed that nuts lower LDL cholesterol levels and improve insulin sensitivity and blood vessel integrity328.
Edible seeds also contain a diverse range of phytochemicals with beneficial biological activities, such as antioxidant, anti-inflammatory, antidiabetic, and anti-tumor effects298 especially when sprouted 329. For example, in an animal model of the neurodegenerative disorder Parkinson’s disease, an extract of pumpkin seed demonstrated antioxidant and anti-inflammatory properties that together improved symptoms 330.
Since nuts and seeds are rich in nutrients, antioxidants, and anti-inflammatory compounds298,328,331, it is recommended to only eliminate them after careful assessment of a genuine need.
A review of various dietary patterns applied to MS concluded that “An appropriate and balanced diet can be extremely helpful in improving the condition and well-being of patients with MS, and effectively support drug therapy” 332. The review paid particular attention to the Mediterranean diet, Mediterranean-DASH intervention for neurodegenerative delay (MIND), intermittent fasting, gluten-free, ketogenic, Paleo, the Wahls, McDougall, and Swank diets, all of which (and more) are described here.
Note that if you are seriously ill and/or on medication, it is generally advised to not make a dramatic dietary change – with the possible exception of giving up ultraprocessed foods – without the care of a professional who knows about nutrition and its effects on health. No less important, it is best to ease into a new program with gradual changes, allowing them to slowly become second nature and the body to adapt to them.
1. Parks NE, Jackson-Tarlton CS, Vacchi L, Merdad R, Johnston BC. Dietary interventions for multiple sclerosis-related outcomes. Cochrane Database Syst Rev. May 19 2020;5:CD004192. doi:10.1002/14651858.CD004192.pub4
2. Kliemann N, Al Nahas A, Vamos EP, et al. Ultra-processed foods and cancer risk: from global food systems to individual exposures and mechanisms. Br J Cancer. Jul 2022;127(1):14-20. doi:10.1038/s41416-022-01749-y
3. Baker P, Friel S. Processed foods and the nutrition transition: evidence from Asia. Obes Rev. Jul 2014;15(7):564-77. doi:10.1111/obr.12174
4. Baker P, Machado P, Santos T, et al. Ultra-processed foods and the nutrition transition: Global, regional and national trends, food systems transformations and political economy drivers. Obes Rev. Dec 2020;21(12):e13126. doi:10.1111/obr.13126
5. Martins AP, Levy RB, Claro RM, Moubarac JC, Monteiro CA. Increased contribution of ultra-processed food products in the Brazilian diet (1987-2009). Rev Saude Publica. Aug 2013;47(4):656-65. doi:10.1590/S0034-8910.2013047004968
6. Moubarac JC, Batal M, Martins AP, et al. Processed and ultra-processed food products: consumption trends in Canada from 1938 to 2011. Can J Diet Pract Res. Spring 2014;75(1):15-21. doi:10.3148/75.1.2014.15
7. Beiki O, Frumento P, Bottai M, Manouchehrinia A, Hillert J. Changes in the Risk of Reaching Multiple Sclerosis Disability Milestones In Recent Decades: A Nationwide Population-Based Cohort Study in Sweden. JAMA Neurol. Jun 1 2019;76(6):665-671. doi:10.1001/jamaneurol.2019.0330
8. Miller FW. The increasing prevalence of autoimmunity and autoimmune diseases: an urgent call to action for improved understanding, diagnosis, treatment, and prevention. Curr Opin Immunol. Feb 2023;80:102266. doi:10.1016/j.coi.2022.102266
9. Walton C, King R, Rechtman L, et al. Rising prevalence of multiple sclerosis worldwide: Insights from the Atlas of MS, third edition. Mult Scler. Dec 2020;26(14):1816-1821. doi:10.1177/1352458520970841
10. Tristan Asensi M, Napoletano A, Sofi F, Dinu M. Low-Grade Inflammation and Ultra-Processed Foods Consumption: A Review. Nutrients. Mar 22 2023;15(6)doi:10.3390/nu15061546
11. Cediel G, Reyes M, Corvalan C, Levy RB, Uauy R, Monteiro CA. Ultra-processed foods drive to unhealthy diets: evidence from Chile. Public Health Nutr. May 2021;24(7):1698-1707. doi:10.1017/S1368980019004737
12. Machado PP, Steele EM, Levy RB, et al. Ultra-processed foods and recommended intake levels of nutrients linked to non-communicable diseases in Australia: evidence from a nationally representative cross-sectional study. BMJ Open. Aug 28 2019;9(8):e029544. doi:10.1136/bmjopen-2019-029544
13. Moubarac JC, Batal M, Louzada ML, Martinez Steele E, Monteiro CA. Consumption of ultra-processed foods predicts diet quality in Canada. Appetite. Jan 1 2017;108:512-520. doi:10.1016/j.appet.2016.11.006
14. Rauber F, da Costa Louzada ML, Steele EM, Millett C, Monteiro CA, Levy RB. Ultra-Processed Food Consumption and Chronic Non-Communicable Diseases-Related Dietary Nutrient Profile in the UK (2008(-)2014). Nutrients. May 9 2018;10(5)doi:10.3390/nu10050587
15. Louzada M, Ricardo CZ, Steele EM, Levy RB, Cannon G, Monteiro CA. The share of ultra-processed foods determines the overall nutritional quality of diets in Brazil. Public Health Nutr. Jan 2018;21(1):94-102. doi:10.1017/S1368980017001434
16. Rauber F, Chang K, Vamos EP, et al. Ultra-processed food consumption and risk of obesity: a prospective cohort study of UK Biobank. Eur J Nutr. Jun 2021;60(4):2169-2180. doi:10.1007/s00394-020-02367-1
17. Hall KD, Ayuketah A, Brychta R, et al. Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake. Cell Metab. Jul 2 2019;30(1):67-77 e3. doi:10.1016/j.cmet.2019.05.008
18. Beslay M, Srour B, Mejean C, et al. Ultra-processed food intake in association with BMI change and risk of overweight and obesity: A prospective analysis of the French NutriNet-Sante cohort. PLoS Med. Aug 2020;17(8):e1003256. doi:10.1371/journal.pmed.1003256
19. Canella DS, Levy RB, Martins AP, et al. Ultra-processed food products and obesity in Brazilian households (2008-2009). PLoS One. 2014;9(3):e92752. doi:10.1371/journal.pone.0092752
20. Canhada SL, Luft VC, Giatti L, et al. Ultra-processed foods, incident overweight and obesity, and longitudinal changes in weight and waist circumference: the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Public Health Nutr. Apr 2020;23(6):1076-1086. doi:10.1017/S1368980019002854
21. Chang K, Khandpur N, Neri D, et al. Association Between Childhood Consumption of Ultraprocessed Food and Adiposity Trajectories in the Avon Longitudinal Study of Parents and Children Birth Cohort. JAMA Pediatr. Sep 1 2021;175(9):e211573. doi:10.1001/jamapediatrics.2021.1573
22. Juul F, Martinez-Steele E, Parekh N, Monteiro CA, Chang VW. Ultra-processed food consumption and excess weight among US adults. Br J Nutr. Jul 2018;120(1):90-100. doi:10.1017/S0007114518001046
23. Mendonca RD, Pimenta AM, Gea A, et al. Ultraprocessed food consumption and risk of overweight and obesity: the University of Navarra Follow-Up (SUN) cohort study. Am J Clin Nutr. Nov 2016;104(5):1433-1440. doi:10.3945/ajcn.116.135004
24. Nardocci M, Leclerc BS, Louzada ML, Monteiro CA, Batal M, Moubarac JC. Consumption of ultra-processed foods and obesity in Canada. Can J Public Health. Feb 2019;110(1):4-14. doi:10.17269/s41997-018-0130-x
25. Vandevijvere S, Jaacks LM, Monteiro CA, et al. Global trends in ultraprocessed food and drink product sales and their association with adult body mass index trajectories. Obes Rev. Nov 2019;20 Suppl 2:10-19. doi:10.1111/obr.12860
26. Schreiner TG, Genes TM. Obesity and Multiple Sclerosis-A Multifaceted Association. J Clin Med. Jun 18 2021;10(12)doi:10.3390/jcm10122689
27. Tsigalou C, Vallianou N, Dalamaga M. Autoantibody Production in Obesity: Is There Evidence for a Link Between Obesity and Autoimmunity? Curr Obes Rep. Sep 2020;9(3):245-254. doi:10.1007/s13679-020-00397-8
28. Ballard ST, Hunter JH, Taylor AE. Regulation of tight-junction permeability during nutrient absorption across the intestinal epithelium. Annu Rev Nutr. 1995;15:35-55. doi:10.1146/annurev.nu.15.070195.000343
29. Fasano A, Shea-Donohue T. Mechanisms of disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. Nat Clin Pract Gastroenterol Hepatol. Sep 2005;2(9):416-22. doi:10.1038/ncpgasthep0259
30. Jeon MK, Klaus C, Kaemmerer E, Gassler N. Intestinal barrier: Molecular pathways and modifiers. World J Gastrointest Pathophysiol. Nov 15 2013;4(4):94-9. doi:10.4291/wjgp.v4.i4.94
31. Nusrat A, Turner JR, Madara JL. Molecular physiology and pathophysiology of tight junctions. IV. Regulation of tight junctions by extracellular stimuli: nutrients, cytokines, and immune cells. Am J Physiol Gastrointest Liver Physiol. Nov 2000;279(5):G851-7. doi:10.1152/ajpgi.2000.279.5.G851
32. Pereira MT, Malik M, Nostro JA, Mahler GJ, Musselman LP. Effect of dietary additives on intestinal permeability in both Drosophila and a human cell co-culture. Dis Model Mech. Nov 28 2018;11(12)doi:10.1242/dmm.034520
33. Lerner A, Matthias T. Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease. Autoimmun Rev. Jun 2015;14(6):479-89. doi:10.1016/j.autrev.2015.01.009
34. Pouzou JG, Costard S, Zagmutt FJ. Probabilistic assessment of dietary exposure to heterocyclic amines and polycyclic aromatic hydrocarbons from consumption of meats and breads in the United States. Food Chem Toxicol. Apr 2018;114:361-374. doi:10.1016/j.fct.2018.02.004
35. Friedman M. Acrylamide: inhibition of formation in processed food and mitigation of toxicity in cells, animals, and humans. Food Funct. Jun 2015;6(6):1752-72. doi:10.1039/c5fo00320b
36. Muncke J. Endocrine disrupting chemicals and other substances of concern in food contact materials: an updated review of exposure, effect and risk assessment. J Steroid Biochem Mol Biol. Oct 2011;127(1-2):118-27. doi:10.1016/j.jsbmb.2010.10.004
37. Popescu M, Feldman TB, Chitnis T. Interplay Between Endocrine Disruptors and Immunity: Implications for Diseases of Autoreactive Etiology. Front Pharmacol. 2021;12:626107. doi:10.3389/fphar.2021.626107
38. Rebolledo-Solleiro D, Castillo Flores LY, Solleiro-Villavicencio H. Impact of BPA on behavior, neurodevelopment and neurodegeneration. Front Biosci (Landmark Ed). Jan 1 2021;26(2):363-400. doi:10.2741/4898
39. Rogers JA, Mishra MK, Hahn J, et al. Gestational bisphenol-A exposure lowers the threshold for autoimmunity in a model of multiple sclerosis. Proc Natl Acad Sci U S A. May 9 2017;114(19):4999-5004. doi:10.1073/pnas.1620774114
40. Hucke S, Eschborn M, Liebmann M, et al. Sodium chloride promotes pro-inflammatory macrophage polarization thereby aggravating CNS autoimmunity. J Autoimmun. Feb 2016;67:90-101. doi:10.1016/j.jaut.2015.11.001
41. Kleinewietfeld M, Manzel A, Titze J, et al. Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature. Apr 25 2013;496(7446):518-22. doi:10.1038/nature11868
42. Zostawa J, Adamczyk J, Sowa P, Adamczyk-Sowa M. The influence of sodium on pathophysiology of multiple sclerosis. Neurol Sci. Mar 2017;38(3):389-398. doi:10.1007/s10072-016-2802-8
43. Martin-Hersog FA, Munoz-Jurado A, Escribano BM, et al. Sodium chloride-induced changes in oxidative stress, inflammation, and dysbiosis in experimental multiple sclerosis. Nutr Neurosci. Jan 2024;27(1):74-86. doi:10.1080/1028415X.2022.2161132
44. Na SY, Janakiraman M, Leliavski A, Krishnamoorthy G. High-salt diet suppresses autoimmune demyelination by regulating the blood-brain barrier permeability. Proc Natl Acad Sci U S A. Mar 23 2021;118(12)doi:10.1073/pnas.2025944118
45. Hernandez AL, Kitz A, Wu C, et al. Sodium chloride inhibits the suppressive function of FOXP3+ regulatory T cells. J Clin Invest. Nov 2 2015;125(11):4212-22. doi:10.1172/JCI81151
46. Wilck N, Matus MG, Kearney SM, et al. Salt-responsive gut commensal modulates TH17 axis and disease. Nature. Nov 30 2017;551(7682):585-589. doi:10.1038/nature24628
47. Kleinewietfeld M, Hafler DA. The plasticity of human Treg and Th17 cells and its role in autoimmunity. Semin Immunol. Nov 15 2013;25(4):305-12. doi:10.1016/j.smim.2013.10.009
48. Wu C, Yosef N, Thalhamer T, et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature. Apr 25 2013;496(7446):513-7. doi:10.1038/nature11984
49. Farez MF, Fiol MP, Gaitan MI, Quintana FJ, Correale J. Sodium intake is associated with increased disease activity in multiple sclerosis. J Neurol Neurosurg Psychiatry. Jan 2015;86(1):26-31. doi:10.1136/jnnp-2014-307928
50. Fitzgerald KC, Vizthum D, Henry-Barron B, et al. Effect of intermittent vs. daily calorie restriction on changes in weight and patient-reported outcomes in people with multiple sclerosis. Mult Scler Relat Disord. Jul 2018;23:33-39. doi:10.1016/j.msard.2018.05.002
51. Nourbakhsh B, Graves J, Casper TC, et al. Dietary salt intake and time to relapse in paediatric multiple sclerosis. J Neurol Neurosurg Psychiatry. Dec 2016;87(12):1350-1353. doi:10.1136/jnnp-2016-313410
52. McDonald J, Graves J, Waldman A, et al. A case-control study of dietary salt intake in pediatric-onset multiple sclerosis. Mult Scler Relat Disord. Mar 2016;6:87-92. doi:10.1016/j.msard.2016.02.011
53. Krementsov DN, Case LK, Hickey WF, Teuscher C. Exacerbation of autoimmune neuroinflammation by dietary sodium is genetically controlled and sex specific. FASEB J. Aug 2015;29(8):3446-57. doi:10.1096/fj.15-272542
54. Altromin. C 1000 - product data sheet - controll diet for rats & mice. Lage: Altromin Spezialfutter GmbH & Co. KG; Undated.
55. University JH. The Mouse. Animal Care and Use Committee. Baltimore: The Johns Hopkins University; Undated.
56. Aubrey A. The Average American Ate (Literally) A Ton This Year. Washington, D.C.: National Public Radio (NPR); 2011.
57. Cogswell ME, Loria CM, Terry AL, et al. Estimated 24-Hour Urinary Sodium and Potassium Excretion in US Adults. JAMA. Mar 27 2018;319(12):1209-1220. doi:10.1001/jama.2018.1156
58. McCarron DA, Kazaks AG, Geerling JC, Stern JS, Graudal NA. Normal range of human dietary sodium intake: a perspective based on 24-hour urinary sodium excretion worldwide. Am J Hypertens. Oct 2013;26(10):1218-23. doi:10.1093/ajh/hpt139
59. Powles J, Fahimi S, Micha R, et al. Global, regional and national sodium intakes in 1990 and 2010: a systematic analysis of 24 h urinary sodium excretion and dietary surveys worldwide. BMJ Open. Dec 23 2013;3(12):e003733. doi:10.1136/bmjopen-2013-003733
60. (NCCIH). NCfCaIH. Green Tea. Health Information Accessed 28 Jan 2022. https://www.nccih.nih.gov/health/green-tea
61. Organization. WH. Guideline: sodium intake for adults and children. World Health Organization. Accessed 10 Apr 2022, https://www.who.int/publications/i/item/9789241504836
62. Chianese R, Coccurello R, Viggiano A, et al. Impact of Dietary Fats on Brain Functions. Curr Neuropharmacol. 2018;16(7):1059-1085. doi:10.2174/1570159X15666171017102547
63. O'Brien JS, Sampson EL. Lipid composition of the normal human brain: gray matter, white matter, and myelin. J Lipid Res. Oct 1965;6(4):537-44.
64. Chan RB, Oliveira TG, Cortes EP, et al. Comparative lipidomic analysis of mouse and human brain with Alzheimer disease. J Biol Chem. Jan 20 2012;287(4):2678-88. doi:10.1074/jbc.M111.274142
65. Cunnane SC, Chouinard-Watkins R, Castellano CA, Barberger-Gateau P. Docosahexaenoic acid homeostasis, brain aging and Alzheimer's disease: Can we reconcile the evidence? Prostaglandins Leukot Essent Fatty Acids. Jan 2013;88(1):61-70. doi:10.1016/j.plefa.2012.04.006
66. Cunnane SC, Schneider JA, Tangney C, et al. Plasma and brain fatty acid profiles in mild cognitive impairment and Alzheimer's disease. J Alzheimers Dis. 2012;29(3):691-7. doi:10.3233/JAD-2012-110629
67. Naudi A, Cabre R, Jove M, et al. Lipidomics of human brain aging and Alzheimer's disease pathology. Int Rev Neurobiol. 2015;122:133-89. doi:10.1016/bs.irn.2015.05.008
68. Swank RL, Goodwin J. Review of MS patient survival on a Swank low saturated fat diet. Nutrition. Feb 2003;19(2):161-2. doi:10.1016/s0899-9007(02)00851-1
69. Daneii P, Neshat S, Mirnasiry MS, et al. Lipids and diastolic dysfunction: Recent evidence and findings. Nutr Metab Cardiovasc Dis. Jun 2022;32(6):1343-1352. doi:10.1016/j.numecd.2022.03.003
70. Prasad M, Rajagopal P, Devarajan N, et al. A comprehensive review on high -fat diet-induced diabetes mellitus: an epigenetic view. J Nutr Biochem. Sep 2022;107:109037. doi:10.1016/j.jnutbio.2022.109037
71. Castro-Alves V, Oresic M, Hyotylainen T. Lipidomics in nutrition research. Curr Opin Clin Nutr Metab Care. Sep 1 2022;25(5):311-318. doi:10.1097/MCO.0000000000000852
72. Berg J, Seyedsadjadi N, Grant R. Saturated Fatty Acid Intake Is Associated With Increased Inflammation, Conversion of Kynurenine to Tryptophan, and Delta-9 Desaturase Activity in Healthy Humans. Int J Tryptophan Res. 2020;13:1178646920981946. doi:10.1177/1178646920981946
73. Steur M, Johnson L, Sharp SJ, et al. Dietary Fatty Acids, Macronutrient Substitutions, Food Sources and Incidence of Coronary Heart Disease: Findings From the EPIC-CVD Case-Cohort Study Across Nine European Countries. J Am Heart Assoc. Dec 7 2021;10(23):e019814. doi:10.1161/JAHA.120.019814
74. Zong G, Li Y, Sampson L, et al. Monounsaturated fats from plant and animal sources in relation to risk of coronary heart disease among US men and women. Am J Clin Nutr. Mar 1 2018;107(3):445-453. doi:10.1093/ajcn/nqx004
75. Sheashea M, Xiao J, Farag MA. MUFA in metabolic syndrome and associated risk factors: is MUFA the opposite side of the PUFA coin? Food Funct. Dec 13 2021;12(24):12221-12234. doi:10.1039/d1fo00979f
76. Pratt DA, Tallman KA, Porter NA. Free radical oxidation of polyunsaturated lipids: New mechanistic insights and the development of peroxyl radical clocks. Acc Chem Res. Jun 21 2011;44(6):458-67. doi:10.1021/ar200024c
77. Zhuang Y, Dong J, He X, et al. Impact of Heating Temperature and Fatty Acid Type on the Formation of Lipid Oxidation Products During Thermal Processing. Front Nutr. 2022;9:913297. doi:10.3389/fnut.2022.913297
78. Lunn JT, H. The health effects of dietary unsaturated fatty acids. Nutrition Bulletin. 2006;31:178-224.
79. Dyall SC, Michael-Titus AT. Neurological benefits of omega-3 fatty acids. Neuromolecular Med. 2008;10(4):219-35. doi:10.1007/s12017-008-8036-z
80. Sullivan D. What to know about omega-6 fatty acids. Medical News Today. Healthline Media; 2020. Accessed September 4, 2022. https://www.medicalnewstoday.com/articles/omega-6-fatty-acids#are-they-healthful
81. Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. Oct 2002;56(8):365-79. doi:10.1016/s0753-3322(02)00253-6
82. Michas G, Micha R, Zampelas A. Dietary fats and cardiovascular disease: putting together the pieces of a complicated puzzle. Atherosclerosis. Jun 2014;234(2):320-8. doi:10.1016/j.atherosclerosis.2014.03.013
83. Dhaka V, Gulia N, Ahlawat KS, Khatkar BS. Trans fats-sources, health risks and alternative approach - A review. J Food Sci Technol. Oct 2011;48(5):534-41. doi:10.1007/s13197-010-0225-8
84. Howarth C, Gleeson P, Attwell D. Updated energy budgets for neural computation in the neocortex and cerebellum. J Cereb Blood Flow Metab. Jul 2012;32(7):1222-32. doi:10.1038/jcbfm.2012.35
85. Kety SS. The general metabolism of the brain in vivo. In: Richter D, ed. Metabolism of the Nervous System. Pergamon; 1957.
86. Nehlig A. Brain uptake and metabolism of ketone bodies in animal models. Prostaglandins Leukot Essent Fatty Acids. Mar 2004;70(3):265-75. doi:10.1016/j.plefa.2003.07.006
87. Mathur D, Lopez-Rodas G, Casanova B, Marti MB. Perturbed glucose metabolism: insights into multiple sclerosis pathogenesis. Front Neurol. 2014;5:250. doi:10.3389/fneur.2014.00250
88. Henneman DH, Altschule MD, Goncz RM, Alexander L. Carbohydrate metabolism in brain disease. I. Glucose metabolism in multiple sclerosis. AMA Arch Neurol Psychiatry. Dec 1954;72(6):688-95. doi:10.1001/archneurpsyc.1954.02330060024004
89. Royds JA, Timperley WR, Taylor CB. Levels of enolase and other enzymes in the cerebrospinal fluid as indices of pathological change. J Neurol Neurosurg Psychiatry. Dec 1981;44(12):1129-35. doi:10.1136/jnnp.44.12.1129
90. Smith KJ, Lassmann H. The role of nitric oxide in multiple sclerosis. Lancet Neurol. Aug 2002;1(4):232-41. doi:10.1016/s1474-4422(02)00102-3
91. Hardonova M, Siarnik P, Sivakova M, et al. Autonomic Nervous System Function in Newly Diagnosed Multiple Sclerosis: Association With Lipid Levels and Insulin Resistance. Physiol Res. Dec 30 2021;70(6):875-882. doi:10.33549/physiolres.934695
92. Oliveira SR, Simao AN, Kallaur AP, et al. Disability in patients with multiple sclerosis: influence of insulin resistance, adiposity, and oxidative stress. Nutrition. Mar 2014;30(3):268-73. doi:10.1016/j.nut.2013.08.001
93. Penesova A, Vlcek M, Imrich R, et al. Hyperinsulinemia in newly diagnosed patients with multiple sclerosis. Metab Brain Dis. Aug 2015;30(4):895-901. doi:10.1007/s11011-015-9665-1
94. Ruiz-Arguelles A, Mendez-Huerta MA, Lozano CD, Ruiz-Arguelles GJ. Metabolomic profile of insulin resistance in patients with multiple sclerosis is associated to the severity of the disease. Mult Scler Relat Disord. Oct 2018;25:316-321. doi:10.1016/j.msard.2018.08.014
95. Sepidarkish M, Kalantari N, Gorgani-Firouzjaee T, Rostami-Mansoor S, Shirafkan H. Association between insulin resistance and multiple sclerosis: a systematic review and meta-analysis. Metab Brain Dis. Jun 2024;39(5):1015-1026. doi:10.1007/s11011-024-01347-2
96. Tomlinson DR, Gardiner NJ. Glucose neurotoxicity. Nat Rev Neurosci. Jan 2008;9(1):36-45. doi:10.1038/nrn2294
97. Qiu WQ, Folstein MF. Insulin, insulin-degrading enzyme and amyloid-beta peptide in Alzheimer's disease: review and hypothesis. Neurobiol Aging. Feb 2006;27(2):190-8. doi:10.1016/j.neurobiolaging.2005.01.004
98. Watson GS, Craft S. Insulin resistance, inflammation, and cognition in Alzheimer's Disease: lessons for multiple sclerosis. J Neurol Sci. Jun 15 2006;245(1-2):21-33. doi:10.1016/j.jns.2005.08.017
99. Muth AK, Park SQ. The impact of dietary macronutrient intake on cognitive function and the brain. Clin Nutr. Jun 2021;40(6):3999-4010. doi:10.1016/j.clnu.2021.04.043
100. Bayer S, Holzapfel C. Carbohydrate intake - current knowledge on weight management. Curr Opin Clin Nutr Metab Care. Jul 1 2022;25(4):265-270. doi:10.1097/MCO.0000000000000840
101. Li L, Shan Z, Wan Z, et al. Associations of lower-carbohydrate and lower-fat diets with mortality among people with prediabetes. Am J Clin Nutr. Jul 6 2022;116(1):206-215. doi:10.1093/ajcn/nqac058
102. Miller JB, Pang E, Broomhead L. The glycaemic index of foods containing sugars: comparison of foods with naturally-occurring v. added sugars. Br J Nutr. Apr 1995;73(4):613-23. doi:10.1079/bjn19950063
103. Cantoni C, Lin Q, Dorsett Y, et al. Alterations of host-gut microbiome interactions in multiple sclerosis. EBioMedicine. Feb 2022;76:103798. doi:10.1016/j.ebiom.2021.103798
104. Guggenmos J, Schubart AS, Ogg S, et al. Antibody cross-reactivity between myelin oligodendrocyte glycoprotein and the milk protein butyrophilin in multiple sclerosis. J Immunol. Jan 1 2004;172(1):661-8. doi:10.4049/jimmunol.172.1.661
105. Hvatum M, Kanerud L, Hallgren R, Brandtzaeg P. The gut-joint axis: cross reactive food antibodies in rheumatoid arthritis. Gut. Sep 2006;55(9):1240-7. doi:10.1136/gut.2005.076901
106. Li J, Yan H, Chen H, et al. The Pathogenesis of Rheumatoid Arthritis is Associated with Milk or Egg Allergy. N Am J Med Sci. Jan 2016;8(1):40-6. doi:10.4103/1947-2714.175206
107. Gargano D, Appanna R, Santonicola A, et al. Food Allergy and Intolerance: A Narrative Review on Nutritional Concerns. Nutrients. May 13 2021;13(5)doi:10.3390/nu13051638
108. Barnard ND, Leroy F. Children and adults should avoid consuming animal products to reduce risk for chronic disease: YES. Am J Clin Nutr. Oct 1 2020;112(4):926-930. doi:10.1093/ajcn/nqaa235
109. Platt DJ, Lawrence D, Rodgers R, et al. Transferrable protection by gut microbes against STING-associated lung disease. Cell Rep. May 11 2021;35(6):109113. doi:10.1016/j.celrep.2021.109113
110. Markowiak P, Slizewska K. Effects of Probiotics, Prebiotics, and Synbiotics on Human Health. Nutrients. Sep 15 2017;9(9)doi:10.3390/nu9091021
111. Mathew P, Pfleghaar JL. Egg Allergy. StatPearls. 2022.
112. Irawan A, Ningsih N, Hafizuddin, et al. Supplementary n-3 fatty acids sources on performance and formation of omega-3 in egg of laying hens: a meta-analysis. Poult Sci. Jan 2022;101(1):101566. doi:10.1016/j.psj.2021.101566
113. Mens AJW, van Krimpen MM, Kar SK, Guiscafre FJ, Sijtsma L. Enriching table eggs with n-3 polyunsaturated fatty acids through dietary supplementation with the phototrophically grown green algae Nannochloropsis limnetica: effects of microalgae on nutrient retention, performance, egg characteristics and health parameters. Poult Sci. Jun 2022;101(6):101869. doi:10.1016/j.psj.2022.101869
114. Vlaicu PA, Panaite TD, Turcu RP. Enriching laying hens eggs by feeding diets with different fatty acid composition and antioxidants. Sci Rep. Oct 19 2021;11(1):20707. doi:10.1038/s41598-021-00343-1
115. Chunder R, Weier A, Maurer H, et al. Antibody cross-reactivity between casein and myelin-associated glycoprotein results in central nervous system demyelination. Proc Natl Acad Sci U S A. Mar 8 2022;119(10):e2117034119. doi:10.1073/pnas.2117034119
116. Reindl M, Waters P. Myelin oligodendrocyte glycoprotein antibodies in neurological disease. Nat Rev Neurol. Feb 2019;15(2):89-102. doi:10.1038/s41582-018-0112-x
117. Johns TG, Bernard CC. The structure and function of myelin oligodendrocyte glycoprotein. J Neurochem. Jan 1999;72(1):1-9. doi:10.1046/j.1471-4159.1999.0720001.x
118. Fakih R, Diaz-Cruz C, Chua AS, et al. Food allergies are associated with increased disease activity in multiple sclerosis. J Neurol Neurosurg Psychiatry. Jun 2019;90(6):629-635. doi:10.1136/jnnp-2018-319301
119. Stefferl A, Schubart A, Storch M, et al. Butyrophilin, a milk protein, modulates the encephalitogenic T cell response to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis. J Immunol. Sep 1 2000;165(5):2859-65. doi:10.4049/jimmunol.165.5.2859
120. Docena GH, Fernandez R, Chirdo FG, Fossati CA. Identification of casein as the major allergenic and antigenic protein of cow's milk. Allergy. Jun 1996;51(6):412-6. doi:10.1111/j.1398-9995.1996.tb04639.x
121. Coucke F. Food intolerance in patients with manifest autoimmunity. Observational study. Autoimmun Rev. Nov 2018;17(11):1078-1080. doi:10.1016/j.autrev.2018.05.011
122. Jung CH, Choi KM. Impact of High-Carbohydrate Diet on Metabolic Parameters in Patients with Type 2 Diabetes. Nutrients. Mar 24 2017;9(4)doi:10.3390/nu9040322
123. Fernandez-Rico S, Mondragon ADC, Lopez-Santamarina A, et al. A2 Milk: New Perspectives for Food Technology and Human Health. Foods. Aug 9 2022;11(16)doi:10.3390/foods11162387
124. Jonnalagadda SS, Harnack L, Liu RH, et al. Putting the whole grain puzzle together: health benefits associated with whole grains--summary of American Society for Nutrition 2010 Satellite Symposium. J Nutr. May 2011;141(5):1011S-22S. doi:10.3945/jn.110.132944
125. Lefevre M, Jonnalagadda S. Effect of whole grains on markers of subclinical inflammation. Nutr Rev. Jul 2012;70(7):387-96. doi:10.1111/j.1753-4887.2012.00487.x
126. Andersson A, Tengblad S, Karlstrom B, et al. Whole-grain foods do not affect insulin sensitivity or markers of lipid peroxidation and inflammation in healthy, moderately overweight subjects. J Nutr. Jun 2007;137(6):1401-7. doi:10.1093/jn/137.6.1401
127. Brownlee IA, Moore C, Chatfield M, et al. Markers of cardiovascular risk are not changed by increased whole-grain intake: the WHOLEheart study, a randomised, controlled dietary intervention. Br J Nutr. Jul 2010;104(1):125-34. doi:10.1017/S0007114510000644
128. Giacco R, Clemente G, Cipriano D, et al. Effects of the regular consumption of wholemeal wheat foods on cardiovascular risk factors in healthy people. Nutr Metab Cardiovasc Dis. Mar 2010;20(3):186-94. doi:10.1016/j.numecd.2009.03.025
129. Katcher HI, Legro RS, Kunselman AR, et al. The effects of a whole grain-enriched hypocaloric diet on cardiovascular disease risk factors in men and women with metabolic syndrome. Am J Clin Nutr. Jan 2008;87(1):79-90. doi:10.1093/ajcn/87.1.79
130. Tighe P, Duthie G, Vaughan N, et al. Effect of increased consumption of whole-grain foods on blood pressure and other cardiovascular risk markers in healthy middle-aged persons: a randomized controlled trial. Am J Clin Nutr. Oct 2010;92(4):733-40. doi:10.3945/ajcn.2010.29417
131. Wolever TM, Gibbs AL, Mehling C, et al. The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein. Am J Clin Nutr. Jan 2008;87(1):114-25. doi:10.1093/ajcn/87.1.114
132. Kyro C, Skeie G, Dragsted LO, et al. Intake of whole grain in Scandinavia: intake, sources and compliance with new national recommendations. Scand J Public Health. Feb 2012;40(1):76-84. doi:10.1177/1403494811421057
133. Fardet A. New hypotheses for the health-protective mechanisms of whole-grain cereals: what is beyond fibre? Nutr Res Rev. Jun 2010;23(1):65-134. doi:10.1017/S0954422410000041
134. de Punder K, Pruimboom L. The dietary intake of wheat and other cereal grains and their role in inflammation. Nutrients. Mar 12 2013;5(3):771-87. doi:10.3390/nu5030771
135. Cianferoni A. Wheat allergy: diagnosis and management. J Asthma Allergy. 2016;9:13-25. doi:10.2147/JAA.S81550
136. Tatham AS, Shewry PR. Allergens to wheat and related cereals. Clin Exp Allergy. Nov 2008;38(11):1712-26. doi:10.1111/j.1365-2222.2008.03101.x
137. Singh P, Arora A, Strand TA, et al. Global Prevalence of Celiac Disease: Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol. Jun 2018;16(6):823-836 e2. doi:10.1016/j.cgh.2017.06.037
138. Neuhausen SL, Steele L, Ryan S, et al. Co-occurrence of celiac disease and other autoimmune diseases in celiacs and their first-degree relatives. J Autoimmun. Sep 2008;31(2):160-5. doi:10.1016/j.jaut.2008.06.001
139. Troncone R, Jabri B. Coeliac disease and gluten sensitivity. J Intern Med. Jun 2011;269(6):582-90. doi:10.1111/j.1365-2796.2011.02385.x
140. Shewry PR. Wheat. J Exp Bot. 2009;60(6):1537-53. doi:10.1093/jxb/erp058
141. Biesiekierski JR, Newnham ED, Irving PM, et al. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. Mar 2011;106(3):508-14; quiz 515. doi:10.1038/ajg.2010.487
142. Sapone A, Bai JC, Ciacci C, et al. Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC Med. Feb 7 2012;10:13. doi:10.1186/1741-7015-10-13
143. Lammers KM, Khandelwal S, Chaudhry F, et al. Identification of a novel immunomodulatory gliadin peptide that causes interleukin-8 release in a chemokine receptor CXCR3-dependent manner only in patients with coeliac disease. Immunology. Mar 2011;132(3):432-40. doi:10.1111/j.1365-2567.2010.03378.x
144. Harris KM, Fasano A, Mann DL. Cutting edge: IL-1 controls the IL-23 response induced by gliadin, the etiologic agent in celiac disease. J Immunol. Oct 1 2008;181(7):4457-60. doi:10.4049/jimmunol.181.7.4457
145. Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol. Feb 2012;42(1):71-8. doi:10.1007/s12016-011-8291-x
146. van Elburg RM, Uil JJ, Mulder CJ, Heymans HS. Intestinal permeability in patients with coeliac disease and relatives of patients with coeliac disease. Gut. Mar 1993;34(3):354-7. doi:10.1136/gut.34.3.354
147. Drago S, El Asmar R, Di Pierro M, et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol. Apr 2006;41(4):408-19. doi:10.1080/00365520500235334
148. Sander GR, Cummins AG, Henshall T, Powell BC. Rapid disruption of intestinal barrier function by gliadin involves altered expression of apical junctional proteins. FEBS Lett. Aug 29 2005;579(21):4851-5. doi:10.1016/j.febslet.2005.07.066
149. Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. Br J Nutr. Mar 2000;83(3):207-17. doi:10.1017/s0007114500000271
150. Hadjivassiliou M, Grunewald R, Sharrack B, et al. Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics. Brain. Mar 2003;126(Pt 3):685-91. doi:10.1093/brain/awg050
151. Thomsen HL, Jessen EB, Passali M, Frederiksen JL. The role of gluten in multiple sclerosis: A systematic review. Mult Scler Relat Disord. Jan 2019;27:156-163. doi:10.1016/j.msard.2018.10.019
152. Pusztai A, Grant G. Assessment of lectin inactivation by heat and digestion. Methods Mol Med. 1998;9:505-14. doi:10.1385/0-89603-396-1:505
153. Dalla Pellegrina C, Perbellini O, Scupoli MT, et al. Effects of wheat germ agglutinin on human gastrointestinal epithelium: insights from an experimental model of immune/epithelial cell interaction. Toxicol Appl Pharmacol. Jun 1 2009;237(2):146-53. doi:10.1016/j.taap.2009.03.012
154. Vojdani A, Afar D, Vojdani E. Reaction of Lectin-Specific Antibody with Human Tissue: Possible Contributions to Autoimmunity. J Immunol Res. 2020;2020:1438957. doi:10.1155/2020/1438957
155. Karpova IS. Specific interactions between lectins and red blood cells of Chornobyl cleanup workers as indicator of some late radiation effects. Exp Oncol. Dec 2016;38(4):261-266.
156. Gong T, Wang X, Yang Y, et al. Plant Lectins Activate the NLRP3 Inflammasome To Promote Inflammatory Disorders. J Immunol. Mar 1 2017;198(5):2082-2092. doi:10.4049/jimmunol.1600145
157. Bakhshi S, Shamsi S. MCC950 in the treatment of NLRP3-mediated inflammatory diseases: Latest evidence and therapeutic outcomes. Int Immunopharmacol. Feb 3 2022;106:108595. doi:10.1016/j.intimp.2022.108595
158. Petroski W, Minich DM. Is There Such a Thing as "Anti-Nutrients"? A Narrative Review of Perceived Problematic Plant Compounds. Nutrients. Sep 24 2020;12(10)doi:10.3390/nu12102929
159. Alasalvar C, Chang SK, Bolling B, Oh WY, Shahidi F. Specialty seeds: Nutrients, bioactives, bioavailability, and health benefits: A comprehensive review. Compr Rev Food Sci Food Saf. May 2021;20(3):2382-2427. doi:10.1111/1541-4337.12730
160. Chavez-Mendoza C, Sanchez E. Bioactive Compounds from Mexican Varieties of the Common Bean (Phaseolus vulgaris): Implications for Health. Molecules. Aug 17 2017;22(8)doi:10.3390/molecules22081360
161. Dueñas M, Sarmentoa, T., Aguileraa, Y., Beniteza, V., Molláa, E., Estebana, R.M., Martín-Cabrejas, M.A. Impact of cooking and germination on phenolic composition and dietary fibre fractions in dark beans (Phaseolus vulgaris L.) and lentils (Lens culinaris L.). LWT - Food Science and Technology. 2016;66:72-78.
162. Hartman TJ, Albert PS, Zhang Z, et al. Consumption of a legume-enriched, low-glycemic index diet is associated with biomarkers of insulin resistance and inflammation among men at risk for colorectal cancer. J Nutr. Jan 2010;140(1):60-7. doi:10.3945/jn.109.114249
163. Masters RC, Liese AD, Haffner SM, Wagenknecht LE, Hanley AJ. Whole and refined grain intakes are related to inflammatory protein concentrations in human plasma. J Nutr. Mar 2010;140(3):587-94. doi:10.3945/jn.109.116640
164. Monk JM, Zhang CP, Wu W, et al. White and dark kidney beans reduce colonic mucosal damage and inflammation in response to dextran sodium sulfate. J Nutr Biochem. Jul 2015;26(7):752-60. doi:10.1016/j.jnutbio.2015.02.003
165. Kumar S, Pandey G. Biofortification of pulses and legumes to enhance nutrition. Heliyon. Mar 2020;6(3):e03682. doi:10.1016/j.heliyon.2020.e03682
166. Xu B, Chang SK. Total Phenolic, Phenolic Acid, Anthocyanin, Flavan-3-ol, and Flavonol Profiles and Antioxidant Properties of Pinto and Black Beans ( Phaseolus vulgaris L.) as Affected by Thermal Processing. J Agric Food Chem. Jun 10 2009;57(11):4754-4764. doi:10.1021/jf900695s
167. Das A, Parida, S.K. Advances in biotechnological applications in three important food legumes. Plant Biotechnology Reports. 2014;8(2):83-99.
168. Sreerama YN, Takahashi Y, Yamaki K. Phenolic antioxidants in some Vigna species of legumes and their distinct inhibitory effects on alpha-glucosidase and pancreatic lipase activities. J Food Sci. Sep 2012;77(9):C927-33. doi:10.1111/j.1750-3841.2012.02848.x
169. Xu B, Chang SK. Reduction of antiproliferative capacities, cell-based antioxidant capacities and phytochemical contents of common beans and soybeans upon thermal processing. Food Chem. Dec 1 2011;129(3):974-81. doi:10.1016/j.foodchem.2011.05.057
170. Djordjevic TM, Šiler-Marinkovic, S.S., Dimitrijevic-Brankovic, S.I. Antioxidant Activity and Total Phenolic Content in Some Cereals and Legumes. Int J Food Prop. 2011;14(1):175-184.
171. Bardocz S, Grant G, Ewen SW, et al. Reversible effect of phytohaemagglutinin on the growth and metabolism of rat gastrointestinal tract. Gut. Sep 1995;37(3):353-60. doi:10.1136/gut.37.3.353
172. Herzig KH, Bardocz S, Grant G, Nustede R, Folsch UR, Pusztai A. Red kidney bean lectin is a potent cholecystokinin releasing stimulus in the rat inducing pancreatic growth. Gut. Sep 1997;41(3):333-8. doi:10.1136/gut.41.3.333
173. Kik MJ, Rojer JM, Mouwen JM, Koninkx JF, van Dijk JE, van der Hage MH. The interaction between plant lectins and the small intestinal epithelium: a primary cause of intestinal disturbance. Vet Q. Apr 1989;11(2):108-15. doi:10.1080/01652176.1989.9694207
174. Lorenzsonn V, Olsen WA. In vivo responses of rat intestinal epithelium to intraluminal dietary lectins. Gastroenterology. May 1982;82(5 Pt 1):838-48.
175. Vasconcelos IM, Oliveira JT. Antinutritional properties of plant lectins. Toxicon. Sep 15 2004;44(4):385-403. doi:10.1016/j.toxicon.2004.05.005
176. Weinman MD, Allan CH, Trier JS, Hagen SJ. Repair of microvilli in the rat small intestine after damage with lectins contained in the red kidney bean. Gastroenterology. Nov 1989;97(5):1193-204. doi:10.1016/0016-5085(89)91690-9
177. Banwell JG, Boldt DH, Meyers J, Weber FL, Jr. Phytohemagglutinin derived from red kidney bean (Phaseolus vulgaris): a cause for intestinal malabsorption associated with bacterial overgrowth in the rat. Gastroenterology. Mar 1983;84(3):506-15.
178. Apfelthaler C, Skoll K, Ciola R, Gabor F, Wirth M. A doxorubicin loaded colloidal delivery system for the intravesical therapy of non-muscle invasive bladder cancer using wheat germ agglutinin as targeter. Eur J Pharm Biopharm. Sep 2018;130:177-184. doi:10.1016/j.ejpb.2018.06.028
179. Bhutia SK, Panda PK, Sinha N, et al. Plant lectins in cancer therapeutics: Targeting apoptosis and autophagy-dependent cell death. Pharmacol Res. Jun 2019;144:8-18. doi:10.1016/j.phrs.2019.04.001
180. Farkas E. [Fermented wheat germ extract in the supportive therapy of colorectal cancer]. Orv Hetil. Sep 11 2005;146(37):1925-31. Szupportiv kezeles fermentalt buzacsira-kivonattal colorectalis carcinomaban.
181. Mishra A, Behura A, Mawatwal S, et al. Structure-function and application of plant lectins in disease biology and immunity. Food Chem Toxicol. Dec 2019;134:110827. doi:10.1016/j.fct.2019.110827
182. Chon SU. Total polyphenols and bioactivity of seeds and sprouts in several legumes. Curr Pharm Des. 2013;19(34):6112-24. doi:10.2174/1381612811319340005
183. Zhu F, Du B, Xu B. Anti-inflammatory effects of phytochemicals from fruits, vegetables, and food legumes: A review. Crit Rev Food Sci Nutr. May 24 2018;58(8):1260-1270. doi:10.1080/10408398.2016.1251390
184. Kennedy AM. Food Allergy. Br Med J. May 2 1936;1(3930):869-74. doi:10.1136/bmj.1.3930.869
185. Jonez HD. The allergic aspects of multiple sclerosis. Calif Med. Nov 1953;79(5):376-80.
186. Chan ES, Greenhawt MJ, Fleischer DM, Caubet JC. Managing Cross-Reactivity in Those with Peanut Allergy. J Allergy Clin Immunol Pract. Feb 2019;7(2):381-386. doi:10.1016/j.jaip.2018.11.012
187. Cochard MM, Eigenmann, P.A. Allergies to Nuts and Seeds. Nuts and Seeds in Health and Disease Prevention. Elsevier; 2011:137-143:chap 15.
188. Ros E. Health benefits of nut consumption. Nutrients. Jul 2010;2(7):652-82. doi:10.3390/nu2070683
10.3390/nu2070652
189. Ros E, Singh A, O'Keefe JH. Nuts: Natural Pleiotropic Nutraceuticals. Nutrients. Sep 19 2021;13(9)doi:10.3390/nu13093269
190. Gan R, Lui, W., Wu, K., Chan, C., Dai, S., Sui, Z., Corke, H. Bioactive compounds and bioactivities of germinated edible seeds and sprouts: An updated review. Trends in Food Science and Technology. 2017;59:1-14.
191. Saleem U, Shehzad A, Shah S, et al. Antiparkinsonian activity of Cucurbita pepo seeds along with possible underlying mechanism. Metab Brain Dis. Aug 2021;36(6):1231-1251. doi:10.1007/s11011-021-00707-6
192. Samtiya M, Acharya S, Pandey KK, Aluko RE, Udenigwe CC, Dhewa T. Production, Purification, and Potential Health Applications of Edible Seeds' Bioactive Peptides: A Concise Review. Foods. Nov 4 2021;10(11)doi:10.3390/foods10112696
193. Zielinska M, Michonska I. Effectiveness of various diet patterns among patients with multiple sclerosis. Postep Psychiatr Neurol. Mar 2023;32(1):49-58. doi:10.5114/ppn.2023.127246
You must be logged in to post a comment.