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Constipation is uncomfortable. Depression can be downright disabling. So imagine the compromised quality of life for people living with both. In fact. According to a Columbia University press release announcing new findings about the connection between these two issues, as much as a third of people with depression experience chronic constipation, and some of these individuals describe their “bowel difficulties as one of the biggest factors reducing their quality of life.”

It’s long been believed that some cases of depression result from low serotonin in the brain. Being that serotonin also plays a key role in gut motility and that the gut is heavily reliant on neurotransmitters for proper function (it’s often called “the second brain”), low serotonin may be contributing to constipation, at least in some individuals.

Researchers at Columbia and Duke Universities looked more closely at this, using mice with a genetic mutation that impairs serotonin production in both the brain and the gut. (The mutation is in the enzyme tryptophan hydroxylase 2, which is the rate-limiting step in the biosynthesis of tryptophan.) The mutation reduces serotonin levels by 60–80% in the central nervous system and induces depressive symptoms in the mice. Affected mice show fewer neurons in the gut, deterioration of the gut lining, and slower bowel transit time.

In their study, “Effects of Serotonin and Slow-release 5-HTP on Gastrointestinal Motility in a Mouse Model of Depression,” researchers gave the mice a slow-release form of 5-HTP, the precursor to serotonin, and this resulted in an increase in the number of neurons in the gut—actually, the number was restored to normal. Gut serotonin levels were also increased, and perhaps the most encouraging finding—if future research shows this translates to humans with constipation—is that gut motility returned to normal. This is one of the first studies to show that neurogenesis in the gut is possible, which may have encouraging implications for treating constipation in general, and in the elderly in particular, who typically experience a loss of GI neurons during aging.

Obviously, 5-HTP has long been available as a supplement. The difference here is that the immediate-release form has not been shown to be effective for GI issues, but the slow-release form may get around this obstacle by providing a more constant supply of the compound. However, there are conflicts of interest that are worth noting among the researchers. Some of the study authors have a patent or a pending patent application on slow-release 5-HTP drugs and hold equity in a company founded to develop these drugs. This may have no implications in terms of bias in the study findings, but it’s important to be aware of nonetheless.

Depression and constipation are both conditions that may be caused by a number of factors besides low serotonin. Reduced serotonin synthesis is especially interesting as an etiological factor because it’s a single element that contributes to both. Hypothyroidism is another issue that should be explored when depression and chronic constipation occur together, particularly if other signs and symptoms of suboptimal thyroid home levels are present. Iodine is the nutrient that comes to mind first when thinking about hypothyroidism, but there are important roles for iron and vitamin A, too.

It’s important to be aware that conventional thyroid testing, which often includes only TSH or TSH and T4, may miss patients who do, indeed, have altered thyroid hormone levels. (See here for a past article looking at this issue.) Regarding constipation, we’ve previously explored lifestyle changes that can help improve bowel function and regularity. Fiber is a contentious issue for those with constipation. It makes sense on the surface that increasing stool bulk should “get things moving,” but this advice sometimes backfires and actually makes things worse. For those with constipation caused by low serotonin or some other factor that slows transit time, adding additional material to be excreted means that more stool may accumulate and stagnate in the colon—exactly the opposite of what anyone with chronic constipation would want to experience. (Magnesium citrate is often helpful for alleviating constipation.)

As always in functional medicine, it’s critical to uncover the root causes of physiological dysfunction and address those, rather than masking the symptoms. For patients with constipation and depression secondary to low serotonin, new forms of 5-HTP may be beneficial, but research remains to be done to substantiate this in humans.

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As discussed in an earlier blog, allulose is the new sweetener on the block, having been introduced to the market in 2015. It offers very palatable sweetness but without the use of sugar or unhealthy, chemically-synthesized sugar substitutes. Further, it is easy on the gastrointestinal tract and provides some positive metabolic effects such as improved glucose tolerance and insulin sensitivity, antioxidant activities, and hypolipidemic actions.

For those embarking on ketogenic and low-carb diets, allulose seems like a sweet savior. However, the U.S. Food and Drug Administration (FDA) had initially confused consumers by requiring that allulose be listed as a sugar in the Nutrition Facts panel on food labels. Lack of name recognition had contributed to the confusion and left consumers to simply assume allulose is another form of sugar because after all, it bears the characteristic suffix “-ose” that identifies all sugars.

The Problem of the Past

Although it was initially thrown into the same camp as sucrose, allulose isn’t biochemically or metabolically similar to sucrose. Allulose is not metabolized by the body and at only 0.4 calories per gram, it possesses only 1/10th the calories of sucrose. Unlike sucrose, allulose does not promote dental decay, nor trigger a normal glucose and insulin response.

Unfortunately, the stipulations of the FDA’s 2016 Nutrition Facts label rule made it impossible to reflect these health benefits of allulose. Instead, allulose had to be included under the “Total Carbohydrate,” “Total Sugars,” and “Added Sugars” sections of the Nutrition Facts label. Further, as an “added sugar,” the caloric value assigned to allulose had to be calculated by the same standard as other added sugars, meaning each gram of allulose in a product had to be reflected as an additional 4 calories, despite the ‘real’ caloric value of allulose. Consequently, these rules had created a dilemma for food and supplement manufacturers who were using allulose as a sweetener in reduced-sugar products such as ketogenic and low-carb products. The labels of these products didn’t accurately reflect the product’s benefits, leaving consumers misinformed. Thankfully, this dilemma was corrected.

A New Solution

On April 17, 2019, the FDA made a historic move by declaring food and supplement manufacturers no longer had to include allulose as a sugar on Nutrition and Supplement Facts labels. Under the new enforcement discretion and guidance, allulose is still listed under the “Total Carbohydrate” section because it bears a similar chemical structure to other sugars, but it can now be excluded from the “Total Sugars,” and “Added Sugars” sections on labels. Further, since allulose is no longer considered an added sugar, the caloric value is not calculated as a traditional sugar. Although it will still be added to the total caloric value of the food or supplement product, the value will be revised to reflect a lower calorie count to more accurately reflect the minuscule caloric value of allulose.

According to the FDA, this decision is a step in revising Nutrition Facts and Supplement Facts labels so that consumers can more easily determine the most relevant and useful information. Nutrition labels have been notoriously confusing to most consumers, making many feel as though they need a doctorate degree in nutrition before they can interpret them. Obviously, this lack of clarity hinders consumers from even glancing at nutrition labels and making nutrition-conscious decisions.

Lest anyone mistakenly begin to think that food manufacturers can start including mysterious ingredients in food and supplement products without fully disclosing them to consumers, it is important to note that allulose must still be included on the ingredient list.

Moving forward, it will be important to educate consumers on the health benefits and advantages of allulose – especially (but not exclusively) those committed to following a ketogenic diet. Keto-friendly shakes, bars, and other products supporting a ketogenic lifestyle are beginning to pop up as the demand increases for convenient, keto-friendly alternatives. Therefore, consumers reading ingredients list may wonder at this novel sweetener. 

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Fish oil or krill oil; that is the omega-3 question of the decade. Fish oil certainly has a long history with a plethora of research to validate its health benefits, but suddenly krill oil moves into the neighborhood making claims of superiority and seeming ready to displace the position fish oil has occupied for so long. Many of us consciously or subconsciously operate under the idea that newer is better, which may cause us to side with krill oil, but this philosophy doesn’t always hold water. Maybe the question is not an either/or scenario, but rather, what are the strengths and limitations of each that may warrant the use of both.

The Argument

The argument for choosing either fish oil or krill oil is rooted in studies that suggest krill oil may be more effective at building tissue levels of omega-3 polyunsaturated fatty acids (n-3 PUFA). This conclusion stems from the fact that up to 65 percent of the omega-3 PUFAs in krill oil are esterified as phospholipids (PL) rather than triacylglycerols (TAG), which are the exclusive form found in fish oil. Phospholipids are generally considered to have a higher bioavailability, being the main component of cell membranes, and are more efficiently absorbed by brain tissue, especially.

The Truth About Bioavailability

Even though logic suggests the bioavailability of phospholipid-based omega-3 PUFAs is better than the traditional TAG form, the proof is always in the studies.

This logic was put to the test in an animal study and the results were published earlier this year (2019). Mice were fed either a control diet or one of six DHA (1%, 2%, or 4%) as PL-DHA or TAG-DHA diets for 4 weeks. Both the PL-DHA and TAG-DHA diets resulted in higher DHA concentration in liver, adipose, heart, and eye, but not brain tissue.  However, there was no significant difference in DHA concentration in all tissues between the PL- or TAG-DHA forms. Additionally, all tissue types showed higher levels of EPA PUFAs for both PL-DHA and TAG-DHA diets. According to this study, the PL form of omega-3 PUFAs doesn’t seem to increase DHA and EPA any more significantly than the TAG form.

In another animal study, published in 2018, researchers investigated the effect of oral short-term and long-term administration of krill oil and fish oil on bioavailability in the blood and brain of rats. Rats were given 1000mg of either fish oil, krill oil made by enzyme extraction, krill oil made by solvent extraction, or control. Blood and brain samples were collected after 2, 4, 8, 12, 24, 48 h of oral administration. Rats were then given 500mg daily for 2 weeks of the same test oils or control and then blood and brain samples collected for long-term evaluation. Results showed that PUFA content in the brain was higher in the short-term among rats receiving krill oils. In the long-term, there was a slightly greater level of EPA and DHA in the brains of rats receiving krill oils compared to fish oil, but the difference was not significant. In the long-term, there was no significant difference between blood levels of DHA among rats receiving either krill or fish oils, but those receiving fish oil did show slightly higher blood concentrations of EPA.

Other Metabolic Markers

What about the effects of krill oil or fish oil on metabolic markers such as fasting serum TAG levels, total lipids, phospholipids, cholesterol, cholesteryl esters, non-esterified cholesterol, vitamin D, and fasting glucose? According to an 8-week randomized parallel study of thirty-six healthy subjects aged 18 to 70 years receiving either fish, krill oil or control oil, fasting serum TAG did not change between the groups, blood glucose decreased significantly in the krill group, vitamin D increased significantly in the fish group, and all other markers increased significantly in the krill oil group.

The Benefits of Krill Oil

Krill is distinct from fish oil not only because of its higher phospholipid content, but also because it contains a unique antioxidant profile which includes the powerful antioxidant, astaxanthin. Astaxanthin has been shown to impart significant health benefits on eyes and skin, but also possesses anticancer, antidiabetic, anti-inflammatory, and antioxidant activities. Krill oil also offers a more sustainable form of PUFAs, coming from a large stock of Antarctic crustaceans with a much higher reproduction rate compared to cold-water fish.

The Benefits of Fish Oil

Fish oil still boasts of significantly higher levels of both EPA and DHA, compared to krill oil and although advocates of krill oil argue that bioavailability is better, studies aren’t showing a significant difference, meaning fish oil may still be a superior means of raising the concentrations of these PUFAs. Fish oil can also be easily obtained in clinically relevant doses by consuming cold-water fish. In this way, consumers are also reaping the benefits of other nutrients found in fish including iodine, selenium, taurine, high-quality proteins, and vitamins D and B12. And due to its wide availability, fish oil remains more cost-effective.

Despite being apparent rivals, krill and fish oil may not be mutually exclusive after all. Instead, each may play a role the other cannot fulfill, making their combined use beneficial and even preferred.

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Brain health is on everyone’s mind at some point in their life. After all, the brain is the central command station of the entire body, controlling everything from our thoughts, memory, speech, moods, and the function of nearly every organ system. The brain never stops working; putting in a 24/7 shift for its entire life. The brain is also one of the greatest medical challenges, offering one enigma after another. Despite the puzzles and intricacies of cognitive and mental health, one thing remains agreed upon – the importance of preserving the health of this vital organ.

Nutrition is often overlooked for its role in preserving brain health until it is too late to realize that years of poor dietary habits have finally left their mark, as evidenced by changes in cognition and mental ability.

Nutrition in Early Neurodevelopment

Beginning in infancy, the brain is highly sensitive to its nutritional input. In fact, much of the brain’s developmental and operational trajectory is established before 3 years of age. No single nutrient can assure a long healthy cognitive future, but some nutrients are key players. For example, protein restriction early in life has been linked to smaller brains with reduced RNA and DNA contents, fewer neurons, simpler dendritic and synaptic head architecture, and reduced concentrations of neurotransmitters and growth factors. The significant role of dietary fats in neurodevelopment is logical considering the fact that the neurological system is primary fatty tissues. Long-chain polyunsaturated fatty acids during gestation, lactation, and early childhood have been extensively studied and associated with childhood cognition and attention. They are critical for neurogenesis and neuronal migration, membrane fatty acid composition and fluidity, synaptogenesis, and the function of the monoaminergic, cholinergic, and GABA-ergic neurotransmitter systems. The micronutrients iron, zinc, and iodine have a significant impact on intellectual, executive, and motor function, as well as learning, attention, memory, and mood. In our effort to maximize brain health and ensure a positive trajectory for much of the population, we must begin with considering the nutritional input during the initial years of life since these are the most formative years, cognitively speaking.

Nutrition and Mid-Life Psychiatry

It is no secret that psychiatric health is becoming more prominent at earlier ages as we witness increasing numbers of teenagers and young adults relying on antidepressants and anxiolytic drugs. Nutrition is one component of these sometimes-debilitating conditions that we fail to consider. According to a review in Clinical Psychological Science, “Both cross-sectional and longitudinal studies have shown that the more one eats a Western or highly processed diet, the more one is at risk for developing psychiatric symptoms such as depression and anxiety. Conversely, the more one eats a diet rich in fruits and vegetables, high in healthy fats, nuts, and fish, and low in processed food (a Mediterranean-style diet), the more one is protected from developing a mental disorder.” Researchers even acknowledge that poor dietary patterns often precede psychiatric symptoms, indicating some degree of causality. Most of the body’s supply of serotonin is produced in the gastrointestinal tract and strongly modulates vagal communication in the gut-brain axis. This link is also implicated in studies that show probiotic therapy influences levels of anxiety, depression, perceived stress, and one’s mental outlook. Nutrition is vital for maintaining healthy neurotransmitter levels during mid-life when psychiatric symptoms can flood in and take control of life.

Nutrition and Alzheimer’s disease

The requirement for good nutrition in maintaining brain health and cognition continues into late adulthood. Cognitive disorders are a serious problem for the aging population. Some age-related cognitive decline and impairment is linked to micronutrient deficiencies such as the B-vitamin family. Alzheimer’s disease is one of the most common cognitive concerns for the elderly and although most research has focused on genetics, more recent discoveries are linking this form of dementia to nutrition and giving it the nickname, “type-3-diabetes,” as various shared biochemical features exist between diabetes mellitus and Alzheimer’s disease. Insulin has now been discovered to be involved in the formation of the neurofibrillary tangles and amyloid plaques that characterize Alzheimer’s disease. So rather than consider this an unfortunate gift of predisposed genetics and age, it could be that our high-sugar, high-carbohydrate dietary preferences are the silent benefactors behind Alzheimer’s disease. 

As we are reminded of the high position our brain plays in the quality of life we experience, let us be more mindful of the foundational elements that foster the development and function of this extraordinary organ. It’s not an element we can abandon at any point in our lifetime. Nutrition truly plays key roles in brain health from cradle to grave.

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Breast cancer is the most common cancer in the world. Although there has been progress in cancer treatment, triple negative breast cancer remains a challenge, as this form of cancer has a complex biology, a poorer outcome, and does not respond to hormonal therapies. Lipid metabolism is more activated in this form of breast cancer and understanding how bioactive molecules can be targeted and modulated is essential to improving patient outcomes.

The effects of DHA and delta-tocotrienol individually on tumor growth reduction combined with conventional therapies have been largely studied. Now, in a new study published two weeks ago in Nutrients, researchers demonstrated that the combination of DHA and delta-tocotrienol shows promise in breast cancer.

Tocotrienols are specific isomers of vitamin E that have been shown to help reduce inflammation and oxidative stress in chronic disease. In addition, tocotrienol isomers have superior antioxidant, anticancer, and anti-inflammatory effects compared to tocopherol isomers. DHA has been used successfully as an adjunct to cancer treatments, increasing their efficacy without adverse effects. The combination of both of these was weakly investigated; however, it has been described to have a positive synergistic effect.

This study demonstrated that DHA and delta-tocotrienol triggered a reduction in lipid droplet biosynthesis, a marker of breast cancer aggressiveness. This effect was not seen with DHA alone, suggesting that the combination may be what is making the difference. Results of this study may prove beneficial for triple negative breast cancer, demonstrating that cell proliferation can be altered through lipid droplet modulation, and thus, affecting the aggressiveness of the cancer.

DHA is known for inducing reactive oxygen species in breast cancer cells; however, delta-tocotrienol helps to reduce reactive oxygen species due to its powerful antioxidant and anti-inflammatory properties. This further supports the concept that delta-tocotrienol can modulate DHA’s effects on lipid droplet biogenesis.

By Michael Jurgelewicz, DC, DACBN, DCBCN, CNS

Source: Pizato N, Kiffier LFMV, et al.  Omega 3-DHA and Delta-Tocotrienol Modulate Lipid Droplet Biogenesis and Lipophagy in Breast Cancer Cells: the Impact in Cancer Aggressiveness. Nutrients. 2019 May 28; 11(6).

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The month of June is dedicated to raising our awareness of the fact that no one is exempt from the effects of aging, which often include cataracts. We don’t often consider the health of our eyes until that health diminishes or is robbed from us. Only then do we realize we have taken our eyesight for granted. It has often been said that our eyes are “our windows into the soul” but it could also be argued that they are the windows into the world, as well. It is a frightening experience to suddenly realize our windows are increasingly covered in a haze until we can no longer see clearly, or at all. Cataracts are similar to this experience. They begin with a haze or cloudiness that can’t be blinked away, but as it progresses, blindness can set in. Cataracts are the leading cause of blindness worldwide and the second leading cause of visual impairment.

The risk for cataracts begins to increase progressively around the age of 40 years and by 75 years of age, nearly half of all adults have cataracts. Among Caucasians, approximately 70 percent experience cataracts by the time they are 80 years old. Further, as lifespans continue to increase, the prevalence of cataract is expected to rise correspondingly. For example, in 2000, 20.48 million cases of cataracts were reported, but just one decade later a 25 percent increase was noted. Therefore, cataracts can present as a public health problem with numerous implications.

Cataracts affect the lens, which lies just behind the iris and pupil. In normal vision, light passes through a clear lens to the retina where it is converted to neural signals and interpreted by the brain as an image. However, when the lens becomes cloudy from a cataract, the image is hazy. The lens is also responsible for image focus and depth perception. It is comprised of water and neatly arranged protein and fiber molecules.

Cataracts most often occur when the protein molecules begin aggregating, disrupting the organized arrangement that is noted in a healthy lens. When proteins group together, light can no longer pass through clearly as it becomes partially blocked by the protein clumps. Cataracts grow larger as more protein joins the clumps and vision becomes increasingly obstructed. Protein phase separation and disturbance of the alignment of fiber cells in the lens are also potential causes of cataracts.

Cataracts have been associated with diabetes, smoking and alcohol use, and prolonged exposure to ultraviolet sunlight. Increased quantities of reactive oxygen species and the resulting oxidative stress most likely underlies the pathology of cataract formation, which is why it is often associated with aging – a state of increased oxidative damage. The lens fiber cells contain extremely high levels of the antioxidant, glutathione, indicating their propensity toward oxidation and their natural efforts to prevent oxidative damage. Further, glutathione is both produced and reduced in the lens, making it fully functional at its source. Aging individuals show larger quantities of oxidized glutathione compared to the overriding amounts of reduced glutathione in young, healthy individuals, against, giving evidence to the redox activity that occurs in the lens throughout life.

Many researchers suggest a genetic predisposition to cataracts. Specific genes linked to cataract development have not been discovered, but studies of twins and familial associations have suggested that heredity can account for approximately 30 to 60 percent of cataract risk.

If oxidative stress fosters cataract development and progression, antioxidants should go far in helping to prevent cataract formation. One animal study sought to determine the association between consuming antioxidants and cataracts by measuring lens chaperone activity which is altered by oxidative stress. In this study, antioxidant consumption resulted in less severe central opacities, slower stage cataracts, and protected chaperone activity in the lens of selenite cataract rats.

Curcumin, a powerful antioxidant, has been receiving more attention among researchers as a potential anti-cataract agent. Both in vivo and in vitro studies have shown that curcumin decreases the markers of oxidation and significantly increases antioxidant activity, protecting cells from oxidative damage in selenite cataract rats.

With an aging population and a high prevalence of cataracts, it is vital that we continue to focus on promoting and maintaining a high intake of antioxidants, both through the diet and in supplementation. Cataracts are widely recognized as the outcome of oxidative damage in the lens, so antioxidants are the solution to protecting our “windows” to both the soul and the world around us.

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The role of a wholesome, nutrient-rich diet in supporting health and wellbeing is inarguable. However, when preoccupation with one’s food quality, provenance or “purity” shifts from a priority to an all-out obsession, it can actually work against physical, mental and emotional health. This “pathological obsession with healthy eating” is called orthorexia nervosa, and it may be an unfortunate outcome of current messaging regarding healthy diets reaching those who are more susceptible than others to this kind of behavior.

We explored the issue of orthorexia nervosa (ON) in an article a few years back, but research conducted since then has revealed more about this condition that is worth looking at. Having a better understanding of who’s at increased risk and what some of the adverse consequences are can help medical and nutrition professionals identify patients and clients who may need counseling in this area.

Jennifer Mills, an associate professor in the Department of Psychology at Canada’s York University, was lead author on a study that attempted to determine who might be at increased risk for ON. Regarding ON in general, she said it succinctly: “When taken to the extreme, an obsession with clean eating can be a sign that the person is struggling to manage their mental health.”

Not surprisingly, the researchers found positive associations between ON and perfectionism, disordered eating, history of dieting or an eating disorder, poor body image, drive for thinness, obsessive-compulsive traits and psychopathology. It’s difficult to determine exact figures for prevalence of ON because there is no universally agreed upon definition. The authors of a paper in the journal Easting and Weight Disorders who looked for commonalities in definitions and diagnostic criteria noted that in multiple studies, primary diagnostic criteria included some of the following: obsessional or pathological preoccupation with healthy nutrition; emotional consequences of non-adherence to self-imposed nutritional rules (e.g., stress or anxiety); or psychosocial impairments in relevant areas of life as well as malnutrition and weight loss.

The authors provided a good general description of ON: “The pursuit of an ‘extreme dietary purity’ due to an exaggerated focus” on food generated by self-imposed dietary rules intended to promote health, but which may have detrimental consequences on health. Steven Bratman, MD, who coined the term orthorexia nervosa, also explained that extreme diets—initially intended for good, healthy reasons—can lead to malnutrition and/or impairment of daily functioning.

Bratman also wrote:

“Enthusiasm for healthy eating doesn’t become ‘orthorexia’ until a tipping point is reached and enthusiasm transforms into obsession. Orthorexia is an emotionally disturbed, self-punishing relationship with food that involves a progressively shrinking universe of foods deemed acceptable. A gradual constriction of many other dimensions of life occurs so that thinking about healthy food can becomes the central theme of almost every moment of the day, the sword and shield against every kind of anxiety, and the primary source of self-esteem, value and meaning. This may result in social isolation, psychological disturbance and even, possibly, physical harm. To put it another way, the search for healthy eating can become unhealthy.”

There might not be a universally accepted definition for the condition, but that doesn’t mean it’s impossible to identify in an “I know it when I see it” approach, particularly for medical and nutrition professionals who are in a good position to recognize when someone’s dedication to “healthy eating” has gotten to the point that it’s interfering with their daily life and may ultimately be causing worsened health—the opposite of the intended effect.

In the age of social media, it’s impossible to escape messages about food, both subliminal and overt. Respected institutions like the Mayo Clinic tell us about “clean eating,” and we’re told that fasting could “prevent aging.” (Imagine that—preventing aging! Who writes these headlines, anyway?) Other news outlets tell us “sugar is definitely toxic,” and while sugar certainly isn’t a health food, strawberries and cantaloupe are probably not the reasons why as much as 88% of US adults are metabolically unhealthy. “Natural” food has become a marker for piousness and purity, with people’s food choices connotating information about their morality in ways it didn’t in the past.

It would be difficult for anyone not to be affected by these messages in some way. It does seem, however, that some are more susceptible than others to reaching a point where obsession about food quality becomes a primary focus and driving motivation in their life, rather than their food being a means to the end of having a happy and healthy body, mind and spirit. And there’s a difference between orthorexia and simply being concerned about following a healthy diet. In an essay about the distinction, Dr. Bratman wrote, “Healthy diet turns into orthorexia when a boundary is crossed and a person’s relationship with food begins to impair various essential dimensions of human life.”

There are reasons why particular dietary approaches may be best for certain individuals to follow—for example, a low-carb or ketogenic diet for those with type 2 diabetes, or a low FODMAP diet for those with IBS. Beyond medical necessity, people quite reasonably may choose to follow any number of diets to support weight loss, athletic performance, or just overall good health, and none of these indicates someone has a mental health condition. Orthorexia is more of a concern when the physical morphs into the psychological, and self-imposed, arbitrary “food rules” create a prison-like atmosphere in one’s mind giving a false sense of control.

With the ever-growing focus on clean eating and the rise of “food shaming,” it’s important for healthcare professionals to be aware and remain vigilant for orthorexia among their patients. Some patients may not realize they’ve crossed a threshold into dangerous behavior and may need help.

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With the popularity of the ketogenic diet exploding, food manufacturers and nutraceutical companies have begun offering several new food products that can make a ketogenic lifestyle not only manageable but also convenient. However, one of the biggest challenges in creating keto-friendly products revolves around crafting a product with palatable sweetness but without the use of sugar or unhealthy, chemically-synthesized sugar substitutes. New sweetening agents are popping up to solve this problem, but most consumers (and many practitioners) are unfamiliar with these new sweeteners. Allulose is one such substance.

A GI-Friendly Sweetener

Allulose is a monosaccharide epimer of fructose, formally called D-psicose. It’s found naturally in jackfruit, figs, raisins, and maple syrup. Humans lack the enzymes to digest allulose, so it is largely excreted. In one study, approximately 90% of ingested allulose was recovered in urine, with 1.79-5.65% recovered in feces. Even more exciting is the fact that allulose does not induce the unpleasant GI effects which are commonly experienced with sugar alcohols due to its low colonic microbial fermentability. This discovery was made in a rat study which measured fermentability using a hydrogen gas breath test and 35 strains of colonic bacteria. In a non-randomized controlled trial, a GI tolerance test for allulose was conducted and no cases of severe diarrhea or GI symptoms were noted until a high dose of 0.5 g/kg of body weight was reached.

Metabolic Effects of Allulose

Allulose is gaining fame as a functional sugar with positive metabolic effects including hypoglycemic, hypolipidemic, and antioxidant activities. Allusose has no impact on blood glucose or insulin levels when consumed in reasonable amounts, is nearly calorie-free, and has been shown to have a small but notable impact on reducing body fat mass. Therefore, it’s an ideal sweetener for those on ketogenic or reduced carb diets.

Allulose not only has no impact on blood glucose and insulin levels, but may actually improve glucose tolerance and insulin sensitivity, as well as reduce adipocyte inflammation. When allulose is included in a meal containing carbohydrates it has been shown to modulate the postprandial glycemic impact of the meal in both healthy and pre-diabetic subjects. In one study, administration of 5g allulose in tea consumed with a mixed meal (425 calories, 84.5g carbohydrate, 13.3g protein, 3.7g fat) resulted in significant decreases in postprandial glucose and glucose area under the curve compared to the control tea (containing 10mg aspartame).

Similar findings were seen in a study of healthy young subjects given various doses of allulose along with 75g of maltodextrin as a beverage. Compared to taking the maltodextrin alone, the elevations in blood glucose and insulin were suppressed with co-ingestion of 5g or 7.5g of allulose, but not with 2.5g. Suppression of insulin is noteworthy, because owing to the prevalence of metabolic syndrome and other hyperinsulinemic conditions, a reduction in glucose levels at the expense of substantially elevated insulin would be undesirable.

The precise mechanisms by which allulose reduces postprandial glucose excursions is not known for certain, but researchers believe it may be due to inhibition of alpha-glucosidase, an intestinal brush border enzyme that breaks down starch and disaccharides into glucose. Another hypothesis is that allulose may promote hepatic uptake of glucose and accumulation of glycogen, increasing glucose tolerance.

Finally, animal studies provide evidence that allulose may have other potentially beneficial effects, such as suppressed activity of hepatic lipogenic enzymes, resulting in reduced abdominal adipose deposition and triglyceride accumulation in the liver.

Individuals embarking on ketogenic and low-carb diets no longer have to be barred from indulging in delicious and convenient treats. On the contrary, allulose is the new kid on the block that shows promise in improving metabolic pathways rather than just preventing a metabolic derailment. Allulose provides a healthy alternative to the sugar alcohols that are notorious for causing GI disruptions, has a pleasant taste and carries more benefits than just sweetness.

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Like all psychiatric disorders, schizophrenia is a debilitating condition that can result in disability, social stigma, and increased risk for early death from physical illnesses. According to the World Health Organization, schizophrenia affects about 21-23 million people worldwide, with more men than women afflicted. Currently available drugs for this condition may come with undesirable side-effects and are not effective for all patients. With that in mind, alternative or adjunct therapies would be most welcome. 

New research suggests that sulforaphane, a bioactive compound found in cruciferous vegetables, especially broccoli seeds and sprouts, may be beneficial for altering levels of glutathione and glutamate in the brain, which may have an application in those with schizophrenia. Compared to healthy people, those with psychosis have altered levels of glutamate and glutathione in certain brain regions. Researchers have speculated that glutathione may serve as reservoir or storage pool for glutamate and could have an influence on synaptic excitability. Targeting this could have implications for treating schizophrenia.

In an experiment using rat brain cells, researchers chemically inhibited the incorporation of glutamine into glutathione, and this resulted in nerves being more excitable and firing faster, shifting to a pattern akin to that seen in the brains of people with schizophrenia. Doing the opposite—inhibiting release of glutamate via the glutathione cycle decreased cytosolic glutamate and slowed the firing speed.

Some of the same researchers investigated the potential for sulforaphane to alter glutathione levels in the brains of healthy humans, operating under the possibility that this may have a beneficial application for schizophrenia patients. Subjects (n=9, so a very small study) consumed 100 µmol sulforaphane (as broccoli sprout extract) daily for one week. Blood and urine samples were collected prior to the first dose and within four hours of the final dose. The final measurement indicated that glutathione levels in the brain increased by about 30%. If this was the result of more glutamate being used for the purpose of synthesizing glutathione, it’s possible this could pave the way for further research in using sulforaphane as an addition to other treatments for schizophrenia.

This is all highly preliminary and speculative—there’s no evidence yet that this would be an effective intervention for schizophrenia, but it points to a plausible mechanism that warrants further research in humans afflicted with the condition to determine an optimal effective dose and to ascertain how long treatment would be required before a beneficial effect is seen—if one is seen at all. Certainly, broccoli seed or sprout extract containing sulforaphane has shown promise for other applications, such as fighting head and neck cancer (in animals), potentially slowing progression of prostate cancer, and improving glucose control in patients with type 2 diabetes.

In the meantime, while more research remains to be done, for people looking to try strategies that have shown promise in humans with schizophrenia rather than in already healthy people, or in rat brain cells and petri dishes, dietary interventions may be worth implementing. Evidence suggests that at least in some patients with schizophrenia, the disorder may be a manifestation of gluten intolerance. Gluten intolerance may drive other mental and psychiatric issues as well, to the point that some researchers even coined the phrase “gluten psychosis.” Evidence is mixed on the efficacy of gluten-free diets for improving schizophrenia, however. Some patients show remarkable improvement, while others do not respond to the dietary change.

Ketogenic diets are another approach worth trying. Limited but very encouraging case reports indicate that dietary ketosis can put schizophrenia into apparently complete remission. One such report details the case of a 70-year-old woman who’d lived with visual and auditory hallucinations since the age of 17. She’d been hospitalized at least five times over the prior six years for suicide attempts and increased psychotic symptoms. Her symptoms showed remarkable improvement in a very short time after adopting a ketogenic diet. In a follow-up clinical visit 19 days after initiating the diet, she reported that on the eighth day, she was no longer hearing voices and there was a decrease in visual hallucinations—and this occurred with no change in her medication regimen; the only change was in her diet. Over the course of 12 months, the subject continued the ketogenic diet and had no recurrence of auditory or visual hallucinations, even when there were isolated occurrences of increased carbohydrate intake. Additional positive outcomes from ketogenic diets for schizophrenia have been reported as well.

Ketones and ketogenic diets induce several beneficial molecular changes in the brain and central nervous system that may be responsible for the effects seen in patients with psychiatric disorders. In the specific case of schizophrenia, it’s believed that the influence of ketosis on increasing GABA synthesis and increasing the GABA; glutamate ratio may play a role.

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Inflammatory bowel disease (IBD) is an autoimmune condition where, in most cases, there are multiple triggers chronically stimulating the immune system over a long period of time in multiple ways. When this happens, the immune system becomes overloaded and overwhelmed, losing its ability to function. This, in turn, leads to chronic inflammation and can cause diarrhea and abdominal pain, as well as other debilitating symptoms.

According to a study published last Wednesday in Nature, researchers demonstrated the chemical and molecular events that shift the microbiome and exacerbate disease activity in patients with IBD. Although previous research has shown differences in the gut microbiome in IBD patients, this study investigated how the changes in the microbiome contribute to an inflammatory response.

This study followed 132 individuals for one year, comparing those with Crohn's disease and ulcerative colitis to a control group that did not have IBD. Each individual provided stool samples every two weeks, blood samples every three months, and colon biopsies at the start of the study. A total of 2,965 stool, biopsy, and blood samples were analyzed along with molecular, cellular, and clinical tools to understand the detailed biochemistry of the disease, as it is important to know what bacteria are present and how these bacteria shift as the patient’s symptoms exacerbate or improve.

Results showed that during periods of disease activity, patients with IBD had higher levels of polyunsaturated fatty acids, including adrenate and arachidonate. In addition, nicotinuric acid was found almost exclusively in the stool of patients with IBD, and levels of vitamins B5 and B3 were insufficient in IBD patients. Also, a group of bacteria related to the genus Subdoligranulum commonly found in almost every individual (which had not been previously isolated) was shown to be depleted during inflammation.

Previous research has identified that in healthy people, the gut microbiome is much more stable than those with IBD. Patients with IBD have dramatic shifts in their microbiomes with some bacteria disappearing almost completely at times.

Medication to treat IBD can also affect the microbiome. Individuals who take steroids for part of their treatment have more fluctuations in their microbiome and those who were experiencing a flare-up in their symptoms are more likely to have dramatic fluctuations in their microbiome.

These results further support the functional medicine approach to assess the microbiome regularly in IBD patients in order to take an individualized approach to manipulate the microbiome and keep these patients in remission, especially if medications like corticosteroids can shift the microbiome, leading to an exacerbation of the disease.

High dose probiotics, fish oil, glutamine, and mucilaginous botanicals are helpful in immunomodulation and for their anti-inflammatory properties. Other common nutrient deficiencies seen in these patients include magnesium and vitamin D. A specific carbohydrate diet (SCD) or elimination diet can improve gastrointestinal function and decrease disease activity.

By Michael Jurgelewicz, DC, DACBN, DCBCN, CNS

Source: Jason Lloyd-Price, Cesar Arze, et al. Multi-omics of the gut microbial ecosystem in inflammatory bowel diseases. Nature, 2019; 569 (7758): 655 DOI: 10.1038/s41586-019-1237-9

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