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Exercise can be such a drag, right? You’ve gotta change your clothes, drive to the gym, spend half an hour on the bike or treadmill – maybe even more, then do some lifting, take a shower… If it seems like a huge time commitment to fit exercise into your day, even though you know you “should,” take heart. Research indicates that very short bouts of intense exercise may be more enjoyable than long, slow slogs, and more than that, they’ll get you the same or better results.

Recent research out of Canada’s McMaster University supports this growing body of evidence. In this study, young sedentary males were divided into a sprint interval training (SIT) group, a moderate-intensity continuous training (MICT) group, and a group of non-exercising controls. Both exercise arms called for three sessions weekly for twelve weeks. The SIT protocol called for three twenty-second “all-out” cycle sprints interspersed with 2 minutes of slower cycling; the MICT protocol involved 45 minutes of continuous cycling at ~70% maximal heart rate. Both protocols involved a 2-minute warmup and 3-minute cooldown. In case it’s not clear, the SIT arm required just one minute of all-out intensity during a session whose entirety lasted only ten minutes, five of which were the warmup and cooldown. One minute! Even the most devoted couch potato could do an all-out bike sprint during TV commercials.

The different approaches to exercise resulted in similar effects on insulin sensitivity, skeletal muscle adaptation, and VO2 max (a measure of cardio-metabolic and respiratory fitness). Actually, beneficial effects on insulin sensitivity and skeletal muscle were greater in the SIT group. The study’s conclusion says it all: “Twelve weeks of brief intense interval exercise improved indices of cardiometabolic health to the same extent as traditional endurance training in sedentary men, despite a five-fold lower exercise volume and time commitment.” Basically, if you have an exercise bike or treadmill in your basement or garage, you can get a perfectly good workout done in less time than it would take to drive to the gym. (And if you don’t have equipment like that, you can get a similar effect by going all-out with bodyweight exercises. No gym membership to pay for, and not even any fancy machines to buy … excuses gone.)

Honestly, though, this isn’t really news, right? Intense exercise resulted in metabolic improvements in healthy young men? What a shock! How about something in a population that notoriously struggles with fat loss: post-menopausal women. Let’s throw another wrench in the works: post-menopausal women with type 2 diabetes. In a small cohort of such subjects (average age 69; average BMI 31 kg/m2), a similar comparison of short duration high intensity cycling (60× 8 seconds at 77-85% maximum heart rate, with 12s of active recovery – a total of 20 minutes of exercise) versus a longer bout at lower intensity (40 min at 55-60% of subjects’ individual heart rate) showed that the shorter, more intense activity had greater benefit than the longer session. The exercises were performed twice weekly for 16 weeks, and the study called for no change to the subjects’ diet. According to the results, total body fat decreased and total fat-free mass (muscle, bone, water) increased in both groups, but significant loss of total abdominal and visceral fat mass was observed only among subjects in the high intensity arm. Newsflash: these women lost visceral and abdominal fat with intense exercise requiring a whopping twenty minutes twice a week, and no change to their diet. Imagine what the results might have been with a concomitant lower carb and higher protein dietary intervention.

Of course, any exercise is better than no exercise, and the best exercise to do is the one you enjoy doing, so that you’ll do it regularly and keep it up for the long term. After all, if you just plain don’t enjoy exercise, you’re not going to make it a priority. So it might help to know that among obese young women, subjects in the high intensity interval arm of one study enjoyed their exercise sessions markedly more than those in the moderate intensity continuous training arm. Beneficial effects of short bouts of high intensity training (only twenty minutes per session!) were observed in obese women after just three weeks of three sessions per week. On average, the women lost body fat, gained lean mass, had increases in VO2 max, and had improved insulin sensitivity. Not bad for three hours of exercise over the course of three weeks.

If you’ve been putting off starting an exercise program because of the time commitment, short bursts of high intensity activity might be the ticket to get you moving. You don’t need to train for a marathon. A few minutes a week, properly executed, can get you results.

 

Sources

  1. Gillen JB, Martin BJ, MacInnis MJ, Skelly LE, Tarnopolsky MA, Gibala MJ. Twelve Weeks of Sprint Interval Training Improves Indices of Cardiometabolic Health Similar to Traditional Endurance Training despite a Five-Fold Lower Exercise Volume and Time Commitment. Sandbakk Ø, ed. PLoS ONE. 2016;11(4):e0154075.
  2. Kong Z, Fan X, Sun S, Song L, Shi Q, Nie J. Comparison of High-Intensity Interval Training and Moderate-to-Vigorous Continuous Training for Cardiometabolic Health and Exercise Enjoyment in Obese Young Women: A Randomized Controlled Trial. Sacchetti M, ed. PLoS ONE. 2016;11(7):e0158589.
  3. Maillard F et al. High-intensity interval training reduces abdominal fat mass in postmenopausal women with type 2 diabetes. Diabetes Metab. 2016 Dec;42(6):433-441.
  4. Smith-Ryan AE, Trexler ET, Wingfield H, Blue MNM. Effects of high-intensity interval training on cardiometabolic risk factors in overweight/obese women. Journal of sports sciences. 2016;34(21):2038-2046.
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Dysmenorrhea is one of the most common complaints among young women. Pain starts a few hours before or at the onset of menstruation and often ceases within a few days. The pain can be debilitating, leading to nausea, vomiting, fatigue and diarrhea. Pharmacological therapies are often not effective and have undesirable side effects.

Previous studies have shown that nutrients such as magnesium, calcium and vitamin E may be helpful to treat menstrual pain. Metabolites of prostaglandins and arachidonic acid also play a role in dysmenorrhea, so improving fatty acid ratios in the diet may reduce inflammation leading to a reduction in pain.  Therefore, using these in combination should have synergistic effects.

According to a recent study published in Gynecological Endocrinology, researchers demonstrated that vitamin E and fish oil, in combination or separately, relieve menstrual pain.

In this double-blind, randomized clinical trial, 100 patients ranging from 18 to 25 years of age were randomly assigned to four groups receiving fish oil (180 mg EPA and 120 mg DHA), vitamin E (200 IU), vitamin E and fish oil combination, or placebo daily for 8 weeks. The severity of the pain was measured by a visual analog scale (VAS) at the beginning and end of the study.

The symptoms reported during menses included leaving daily tasks (72%), fatigue (89.8%), nausea (51%), vomiting (31.8%), diarrhea (19.01%), and headache (42.1%).

According to the results, omega-3 and vitamin E supplements significantly reduced menstrual pain compared to placebo. The group that received the combined vitamin E and omega-3s experienced a greater positive effect on menstrual pain compared to the other groups.

Dysmenorrhea is also frequently associated with estrogen dominance; therefore, hormone assessment and support with progesterone, DIM, and/or calcium-d-glucarate may be helpful for balancing the estrogen/progesterone ratio.

By Michael Jurgelewicz, DC, DACBN, DCBCN, CNS

 

Source: Sadeghi N, Paknezhad F, et al. Vitamin E and fish oil, separately or in combination, on treatment of primary dysmenorrhea: a double-blind, randomized clinical trial. Gynecol Endocrinol. 2018 Mar 15:1-5. doi: 10.1080/09513590.2018.1450377

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A new paper exploring the efficacy of a very low carbohydrate diet for the management of type 1 diabetes offers insights that could have powerful implications for the way this condition is treated.

Management of type 1 diabetes (T1D) is fraught with risks for hypoglycemia, ketoacidosis, and other potentially fatal complications. The effects of carbohydrate and protein on blood glucose are not always easy to predict, especially when factoring in other issues that affect gluco-regulation, such as physical activity, stress, and quality and quantity of sleep. Matching insulin doses to the amount of carbs and protein in meals is a delicate balancing act that often fails, leading to postprandial blood sugar highs or lows that keep affected individuals on a dangerous rollercoaster daily. Part of this owes to the underrecognized biological fact that the concentration of insulin required to inhibit glucagon release from pancreatic alpha cells is orders of magnitude greater than the concentration that reaches the liver and the rest of the body (muscle cells and adipocytes). So the amount of injected insulin needed to control postprandial hyperglycemia overshoots what the rest of the body needs, often resulting in hypoglycemia.  

Guidelines for blood sugar control for those with T1D are typically more relaxed than for those with type 2, or for the general public. This owes to the potential for dangerous hypoglycemic events when too much insulin is administered: some doctors and professional organizations err on the side of caution, preferring to recommend slightly lower doses of insulin in order to avoid hypoglycemia, with the understanding that this means random blood sugar measurements as well as HbA1c will tend to run higher than may be most desirable.

Unfortunately, those with T1D are not immune to the long-term adverse outcomes from sustained hyperglycemia, and they also suffer negative consequences from long-term insulin therapy, ultimately ending up with symptoms resembling those of type 2 diabetes (T2D) and insulin resistance: weight gain (especially central adiposity), hypertension, arterial calcification, and dyslipidemia. The presence of insulin resistance characteristic of T2D secondary to long-term insulin therapy in an individual with T1D is known as “double diabetes.” (These people often, but not always, have a family history of type 2.) Intensive management of blood glucose with ever-increasing doses of insulin means that HbA1c improves—but it comes at the expense of increased risk for other health complications.

The old paradigm of “carb up and shoot up” (with insulin) has not served type 1 diabetics well. Obviously, the etiology of T1D is completely different from that of T2D, but carbohydrate restriction may nevertheless be an extremely valuable therapeutic tool for those with T1D.

Unlike type 2 diabetics—many of whom are able to discontinue insulin injections after adopting a low carb or ketogenic diet—those with type 1 will always require some amount of exogenous insulin. However, evidence is mounting that a very low carb diet (VLCD) can significantly reduce the amount needed, and the lower the doses of insulin used, the smaller the margin of error, and the less likelihood there may be for hypoglycemic events.

This was reflected in the paper, published in the journal Pediatrics. The research focused on a cohort of children and adults with T1D who use a VLCD to manage blood glucose, guided by the recommendations in the book, Dr. Bernstein’s Diabetes Solution: The Complete Guide to Achieving Normal Blood Sugars, written by a physician with type 1 diabetes. These individuals are part of a Facebook group, TypeOneGrit, in which a commitment to following Dr. Bernstein’s very low carb guidelines to manage T1D is a stipulation for membership.

Among this cohort, mean daily carbohydrate intake (self-reported, or reported by parents for affected children) was 36 ± 15g, and mean HbA1c was 5.67 ±0.66%. Of the participants who reported continuous glucose monitor readings, average blood glucose was 104 ± 16 mg/dL—quite impressive for those with type 1, especially when you take into account the average daily dose of insulin was 0.40 ± 0.19 units/kg/day—also impressive compared to the amounts many others may require.

Overall, these individuals experienced relatively few hypoglycemic episodes, with 69% experiencing 5 or fewer episodes per month, and 18% experiencing 10 or more. Severe episodes were not absent, however: 2% reported hypoglycemia with seizure or coma and 4% required glucagon administration over the previous year. Very low carb diets may reduce the likelihood of these events, but obviously they cannot eliminate them entirely.

Overall, participants reported high levels of satisfaction with their own diabetes control, but fewer were satisfied with their professional medical care:

“Participants reported high levels of overall health and satisfaction with diabetes management but not with their professional diabetes care […] and 27% did not discuss their adherence to a VLCD with their diabetes care providers. Of those who did discuss their diet, only 49% agreed or strongly agreed that their diabetes care providers were supportive. Narrative explanations by participants for not discussing their diet included disagreement on treatment goals and approach, perceived provider disinterest or unfamiliarity with a VLCD, a desire to avoid conflicts with the provider, and (for parents) fear of being accused of child abuse.”

It's an unfortunate state of affairs when individuals achieve impressive blood sugar management with a strategy well-recognized to do just that, yet they feel they have to “hide” it from their healthcare professionals because it’s unconventional. Before the synthesis of synthetic insulin, carbohydrate restriction was the only viable method to provide even a modicum of improved quality of life for people with T1D. That it has fallen out of favor may be due the availability of insulin as well as the longstanding official government guidelines that demonized dietary fat and encouraged liberal consumption of grains and other carbohydrates.

Evidence indicates that dietary carbohydrate restriction may be “the most effective adjunct to pharmacology in type 1.” Again, to be clear, those with type 1 diabetes will always require exogenous insulin. A VLCD may be an adjunct to, not a substitute for, pharmacological management. 

The paper discussed here has several limitations, which the authors are upfront about. One was the demographics of the cohort: 88% were white, non-Hispanic, and 84% (of the adult participants or the parents responding on behalf of children with T1D) had completed college of the equivalent. So this is not a cross-sample of a wider, more diverse population with T1D, and these individuals were all also highly motivated, as they had already been adhering to a strict low carb diet for a mean of 2.2 ± 2.9 years. Nevertheless, you have to start somewhere, and the findings presented are a warning shot across the bow of those who accept HbA1c still in the diabetic range as desirable or “good enough,” knowing full well the long-term complications of chronic hyperglycemia among type 1 diabetics.

Individuals with type 1 diabetes must always closely monitor their blood glucose and should undertake dietary changes only under the supervision of qualified medical professionals. However, the increasing availability of continuous glucose monitors means that they can see in real time how various foods affect them, and they may be in a better position than ever to use that data to guide their dietary choices. A low carb diet should not be dismissed out of hand:

“…we observed measures of glycemic control in the near-normal range, low rates of hypoglycemia and other adverse events, and generally high levels of satisfaction with health and diabetes control. These findings are without precedent among people with T1DM, revealing a novel approach to the prevention of long-term diabetes complications.”

People living with T1D deserve to know that with the right combination of diet and pharmaceuticals, they can achieve truly normal blood sugar.

By Amy Berger, MS, CNS

 

Related Products: Pure PaleoMeal® Chocolate and Vanilla, PurePaleo™ Chocolate and VanillaPure PaleoBar™, andWheyCool™ Chocolate / UnflavoredVanilla

Related Nutrient Roundtable: Insulin Resistance

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It’s hard to believe that in certain circles, protein has gotten a reputation as being harmful for bone health.  After all, Paleolithic hunter-gatherer diets typically contained a large proportion of meat, yet anthropologists can sometimes distinguish the remains of hunter-gatherers from those of agriculturalists solely by examining the bones: the high-protein eating hunter-gatherers typically had bones that were larger, stronger and denser, and showed fewer signs of chronic disease. 

Scientists believe the differences in physical activity between the two civilizations played a bigger role than any dietary changes, and sure, hunting and gathering no doubt required a lot of time on one’s feet, but ask any farmer: farming isn’t exactly sedentary work!  Even if a heavy physical workload was responsible for Paleolithic peoples’ stronger bones, we can still conclude that a high intake of animal protein didn’t work against building bone mass.    

So how did some people come to think that protein—animal protein, in particular—is harmful for bones?

Yes, Protein is Acidic, But…

The assumption that a high protein intake results in reduced bone mineral density comes primarily from the idea that protein presents an acid load upon digestion, and the body leaches calcium from the bones in order to buffer this acidity in the blood.  This is a great hypothesis on paper.  The problem is, experimental evidence in humans shows that it isn’t actually true.  Or, even if it is true, and protein causes calcium to be released from bone tissue, protein also increases calcium absorption, so the net effect on bone density is still positive—stronger bones. 

It’s true that animal proteins have an acid residue, but so do grains and sugars, yet you rarely hear anyone cautioning people against consuming pasta, rice, bread, and sugary desserts for the sake of their bone health.  (Vegetables and fruits are net alkaline foods, while pure fats and oils are neutral.)  People might cut these carbs out to lose weight or manage their blood sugar, but to protect their bones?  Crickets. 

Let’s take a closer look at the effect of protein consumption on bones. 

Protein is a Net Bone Builder

A systematic review and meta-analysis from no less than the National Osteoporosis Foundation determined that regarding bone health, “Current evidence shows no adverse effects of higher protein intakes.”  Of course, no adverse effects doesn’t necessarily mean higher protein intakes are beneficial; they might be neutral and have no effect one way or the other.  However, numerous studies have shown that higher protein intake is, in fact, beneficial for bone health.    

As long as calcium intake is adequate, higher animal protein intakes are protective against hip fracture among middle-aged men and women.  There is a beneficial effect of animal and dairy protein intake on bone strength and structure.  In healthy post-menopausal women, animal proteins (including dairy) were shown to have a beneficial effect on bone strength and microstructure, with a positive association between protein intake, bone failure load, and stiffness of the peripheral skeleton.

Compared to a diet calling for a daily protein intake of 0.8 grams/kg of body weight—which is typical of most guidelines for protein intake—a diet calling for substantially more—1.4g/kg/day—attenuated bone loss during weight loss in overweight middle-aged adults.  This is in line with mounting evidence that aging individuals should consume more protein, not less

This has been observed over and over again.  According to one review, “consuming protein (including that from meat) higher than current Recommended Dietary Allowance for protein is beneficial to calcium utilization and bone health, especially in the elderly.”

Low protein diets may induce secondary hyperparathyroidism due to reduced intestinal calcium absorption, while a high protein diet was shown to have no effect on serum parathyroid hormone levels.  Another study showed that, among post-menopausal women, a high protein intake did reduce parathyroid hormone levels, coupled with an increase in intestinal calcium absorption, along with higher IGF-1 levels, with no change to biomarkers of bone homeostasis.  The authors concluded, “The increased IGF-I and decreased PTH concentrations in serum, with no change in biomarkers of bone resorption or formation, indicate a high-protein diet has no adverse effects on bone health.”

The bottom line here is, higher protein intakes do cause increased urinary calcium excretion, which is where the acid load idea has its basis.  However—and this is a big however—they also cause increased calcium absorption, and the net effect is increased calcium retention.  Think of it this way: if person A makes $100,000 a year and spends $50,000, they’ll have more money in the bank than person B, who makes $60,000 and spends $30,000.  Even though person A spent more money than person B, they took in more initially, so they still retained more.  Getting back to protein, even if the body excretes more calcium on a higher protein diet, if it also took in more to begin with, the net effect is actually higher calcium retention.   

Moreover, the calcium excreted does not necessarily come from bone stores: “…recent findings do not support the assumption that bone is lost to provide the extra calcium found in urine.”  The excreted calcium may be some of the extra dietary calcium that the body does not require at that time.  (Anyone who absorbs 100% of the nutrients they ingest should offer themselves up as a research subject, because that is some mighty rare digestive efficiency!)

Bones: More Than Just Calcium

Bones aren’t just a conglomeration of minerals wrapped around nothing.  They’re not just calcium, phosphorus, magnesium and other structural elements arranged haphazardly with no scaffolding keeping them in place.  If bones were nothing but calcium, they would shatter anytime someone took a fall, like a piece of chalk dropped on the ground.  To the contrary, according to Roland Kröger, lead author of a recent paper that uncovered new revelations about the fractal organization of bone nanostructure:

“Bone is an intriguing composite of essentially two materials, the flexible protein collagen and the hard mineral called apatite.” (Source)

Being that protein is a primary structural constituent of bone, it’s hard to fathom that consuming protein might lead to weaker bones.  It would be like claiming higher protein diets are counterproductive for building muscle. 

Protein has Multiple Beneficial Effects on Bones

Aside from contributing to the structural integrity of bone, protein exerts an influence on various hormones that affect bone building and resorption.  Here’s the short list:

Takeaway Message

None of this means that anyone needs to go out of their way to gorge on protein, but certainly a reasonable protein intake isn’t harmful for bones.  In fact, post-menopausal women and older individuals of both sexes may be better off increasing their protein intake, rather than steering clear because of unfounded fears about the negative effects on bone density, which have not been substantiated in studies.

 

Related Products: PurePaleo™ Chocolate and Vanilla, Pure PaleoMeal® Chocolate and Vanilla, Pure PaleoBar™, Osteoben, OsteoForce™ Supreme, OsteoForce™

Related Nutrient Roundtable: Bone Support

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Omega-3 fatty acids play an essential role in eye health. While previous research has shown that fish oil supplementation can protect against dry eye syndrome and macular degeneration, a study published last week demonstrated that fish oil supplementation may significantly reduce intraocular pressure, which helps to lower the risk of ocular hypertension and glaucoma. Increased intraocular pressure (IOP) tends to rise in Western populations where there are lower intakes of polyunsaturated fats.

In this study, 105 individuals 18 years of age and older were randomized to take one of the following: a krill oil supplement containing 945 mg/d of EPA and 510 mg/d of DHA, a fish oil supplement containing 1000 mg/d EPA and 500 mg/d DHA, a fish oil supplement containing 900 mg/d EPA and 600 mg/d DHA, an essential fatty acid supplement containing 900 mg/d EPA with 600 mg/d DHA and 900 mg/d ALA, or a placebo supplement containing 1500 mg/d of olive oil for three months. Intraocular pressure was measured at baseline and at the three month follow-up visit.

Results showed that omega-3 fatty acid supplementation significantly reduced intraocular pressure in adults consuming a Western diet. This is the first study that demonstrates that fish oil supplementation can modulate intraocular pressure in humans, which can reduce the need for topical IOP-lowering agents.

Fish oils offer numerous other benefits for eye health. They provide neuroprotective benefits to the sensory peripheral nerves in the cornea and support the function of the retina, which is the area associated with glaucoma and dry eye syndrome.

Additional nutrients and antioxidants that help support eye health include vitamins A, C, D, and E, zinc, lutein, and zeaxanthin.

By Michael Jurgelewicz, DC, DACBN, DCBCN, CNS

 

Source: Downie LE, Vingrys AJ. Oral Omega-3 Supplementation Lowers Intraocular Pressure in Normotensive Adults. Transl Vis Sci Technol. 2018 May 1;7(3):1.

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The human microbiome and gut health has become a crucial focus for practitioners as science continues to uncover its vital importance in health and disease prevention. Most of the attention has been focused on the bacterial species that constitute this microbial environment, but as genetic sequencing technology improves, we are discovering other forms of microbes that play an important role in maintaining or dismantling this delicate environment.

Fungi is beginning to earn some recognition; especially in light of the new wave of health conditions stemming from pathogenic mold exposure. Not all fungal species are harmful. The human microbiome contains some commensal fungi. In fact, over 400 species of fungi have been identified in association with humans and found within the digestive tracts of 70 percent of all healthy adults. Common commensal fungal species that interact with the human microbiome include Candida spp., S. cerevisiae, Phialemonium, Galactomyces, Cladosporium, and Malassezia spp. As with many bacterial species, balancing their quantities is key for health.

Mycotoxins Defined

Mycotoxins are natural, low-molecular-weight secondary fungal metabolites that are detected in various agricultural commodities and humid indoor environments, such as water-damaged buildings. Some of the most common mycotoxins include aflatoxins (AF), sterigmatocystin (ST), fumonisin B (FB), ochratoxins A (OTA), deoxynivalenol (DON), nivalenol (NIV) and T-2 toxin. Most of these mycotoxins originate from common food-borne fungi including, Aspergillus spp., Penicillium spp. and Fusarium spp.

Mycotoxin Dangers

Mycotoxins are receiving more consideration because they have been found to impair the host immune response, increasing susceptibility to other pathogens. More specifically, they trigger the secretion of mucus, antimicrobial peptides and immunoglobulins, and induce intestinal epithelial cells to secrete chemotactic factors and pro-inflammatory cytokines. These responses lead to chronic inflammation in the gastrointestinal tract. Immune suppression (especially cell-mediated immune responses), deficiencies in the humoral immune response, and a reduction in the size of immune tissues and organs are common with mycotoxin exposure, leading to increased susceptibility to infections caused by Salmonella spp., E. coli, Clostridium perfringens, retroviruses, and viruses common in upper respiratory tract infections. Additionally, fungi species and mycotoxins can alter both pathogenic and commensal microbes, increasing the invasiveness and toxicity of pathogens, inhibiting or promoting biofilm formation, and altering the reproductive capacity of all species.

Environmental mycotoxins, most often sourced from water-damaged buildings, are commonly implicated in chronic mucosal disorders and gut dysfunction. They have been found to directly damage the gut epithelial barrier by disrupting junctional proteins, and encouraging cell death. As pathogenic and commensal microbes translocate across the damaged epithelial barrier, inflammation ensues and further exacerbates the situation. Pneumonia and chronic obstructive pulmonary disease are more serious outcomes of exposure to environmental mycotoxins.

Mycotoxins in Gastrointestinal Conditions

Mycotoxins play a significant role in various gastrointestinal conditions. Overgrowth of Candida spp. has long been recognized as a leading factor in dysbiosis and gut permeability, and more recently involved in the pathology of peptic ulcers, giving evidence to the necessity for balance within commensal species. Larger fungal loads, decreased fungal diversity, and antibodies for Saccharomyces cerevisiae have been implicated in Crohn’s disease, while C. albicans increased the frequency of all forms of IBD. Fungal dysbiosis, often resulting from anti-fungal and/or antibiotic therapy, worsened colitis models, exacerbated allergic airway disease, and was a potential cause of antibiotic-associated diarrhea. Both Candida species and Geotrichum candidum, are common in IBS, which improves with anti-fungal treatments such as nystatin.

Studies found that colorectal cancer progression and adenoma size were directly linked to a lack of fungal diversity and the enrichment of specific species such as the order Saccharomycetales and Fusarium. Many mycotoxins, including aflatoxins, have been well-established as carcinogenic, and linked specifically to hepatocellular, gastric, and esophageal carcinomas.

Probiotics

Probiotics and prebiotic compounds have long been used to reestablish and maintain a healthy gut microbiome, but these advantages aren’t just seen among bacterial species. Probiotics and prebiotic compounds can support a shift in fungal biodiversity and decrease the bioaccessibility of mycotoxins as was shown in one study where probiotics reduced the bioaccessibilty of common mycotoxins anywhere from 10 to 57 percent. In another study, Bb. longum, Bb. bifidum, Bb. breve, Bb. adolescentes, Lb. rhamnosus, Lb. casei-casei, S. termofilus, Lb. ruminis, Lb. casei and 22 strains of Saccharomyces cerevisiae were effective against reducing mycotoxins.

In our quest to restore the gut microbiome, let’s not forget the crucial role of fungal species both in the pathogenesis of disease and for maintaining a highly diverse microbial environment in the gut to promote optimal health. Nutraceuticals that target the unique structure of fungi can address overgrowth and pathogenic species, while probiotics are vital for promoting and maintaining a healthy microbiome.

By Nicole Spear, MS, CNS

 

Related Products: GastroMend-HP™, GI Microb-X™

Related Nutirent Roundtable: Designs For Health and Diagnostic Solutions Laboratory Present Advances in Testing of the GI Microbiota

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When listing the most important organs in the body—the ones that do the lion’s share of keeping us alive—people will typically rattle off the heart and brain first. After all, if the heart stops beating, the other organs can’t keep going on their own, and if the brain is dead, someone might technically be “alive,” but it isn’t really much of a life. But the liver tends to get overshadowed by these other two, yet it’s no less important to the healthy functioning of the entire rest of the body.

Considering the rates of cardiovascular disease in the industrialized world, and the growing economic and emotional burdens of Alzheimer’s disease, people are right to have the heart and brain come to mind first when thinking about health. But cases of severe liver disease continue to grow, with 3.9 million adults living with liver disease in the US alone, and over 38,000 deaths annually from chronic liver disease. In 2007, the CDC ranked liver disease as the 12th leading cause of death in the US. With more and more people being diagnosed with NAFLD, hepatitis, cirrhosis and liver cancer, healthcare professionals are on the lookout for natural compounds that can help patients support liver health.

One candidate that deserves consideration is Schisandra chinensis (also called Chinese magnolia vine), the fruit of which is called magnolia berry or five-flavor fruit. The fruit (berries) is the part of the plant typically used in Chinese and botanical medicine, and in Korea it is sometimes enjoyed as a tea. The plant is native to northeastern China, Korea, Japan, and the eastern part of Russia. (Russian scientists were among the first to document the broad applications of Schisandra.)

Schisandra has potent protective effects on the liver, including increasing cytochrome P450 activity, decreasing liver enzymes, and accelerating the proliferation of hepatocytes, which is instrumental for liver repair and regeneration. Chronic alcohol abuse is one of the primary causes of liver damage. In a rat study, treatment with triterpenoid compounds extracted from Schisandra chinensis was shown to reduce alcohol-induced oxidative stress in the liver, and to have a beneficial effect on liver function and histological changes.

Of course, excessive alcohol consumption isn’t the only contributor to liver damage. Another biggie is the obesogenic dietary landscape we live in today. The combination of high carb and high fat—especially with much of that fat coming from omega-6-rich seed oils—takes a toll on the liver. (Fat deposited in the liver is likely one of the early steps in the pathogenesis of type-2 diabetes.) The buildup of fat in the liver of non­-drinkers, or those who consume alcohol only moderately, is so common now that we know it by its own abbreviation: NAFLD, for non-alcoholic fatty liver disease. A low-carb diet can be a frontline intervention for reversing fatty liver, but Schisandra may be a helpful adjunct. In mice in vivo, and in cultured human liver cells in vitro, Schisandra extract was shown to inhibit endoplasmic reticulum stress, which is associated with development of NAFLD.

In a mouse model of NAFLD, compared to untreated mice with fatty liver, fatty liver mice treated with a Schisandra polysaccharide extract showed reductions in serum triglycerides, total cholesterol, LDL-C, ALT and AST of 31.3%, 28.3%, 42.8%, 20.1% and 15.5%, respectively, and HDL-C increased by almost 27%, with a 28% reduction in hepatic triglycerides—not bad! Other mouse studies confirm the lipid-lowering effects of Schisandra, attributing this in part to inhibition of mRNA expression of genes involved in lipogenesis, such as fatty acid synthase and acetyl-CoA carboxylase, as well as inhibition of HMG-CoA reductase—the enzyme targeted by statin drugs.

Beyond alcohol abuse and the detrimental effects of the modern diet, a third major factor contributing to liver damage is acetaminophen toxicity. (In fact, overdose of acetaminophen is the most common cause of acute liver failure.) In a mouse model of acetaminophen-induced hepatotoxicity, acute treatment with Schisandra chinensis (3 hours after acetaminophen administration) protected liver mitochondria and cell viability. Extracts from other Schisandra species have also shown powerful effects against acetaminophen damage: a mouse study showed that pretreatment with various lignans extracted from Schisandra fructus prevented the depletion of hepatic glutathione, and reduced the activity of enzymes involved in detoxification/bioactivation of acetaminophen, resulting in reduced formation of the more toxic intermediate, NAPQI (N-acetyl-p-benzoquinone imine). Extracts from Schisandra sphenanthera have been shown to increase antioxidant capacity, offering a degree of protection against hepatotoxicity, evidenced by reducing the increase in ALT and AST, and preserving hepatic glutathione compared to untreated mice.

 

Related Product: Hepatatone Plus™

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Looking to add more greens to your diet but afraid you’ll completely shut down if you see one more kale chip or spinach salad? Consider chard! Available year-round and in an array of eye-catching colors, chard is a nutritious and hardy green that pops up a lot in rustic Italian cooking, but graces North American tables far less frequently. Not to worry; there are plenty of ways to incorporate chard into your cooking and expand your culinary repertoire.

If chard stalks and leaves remind you of beet greens, with their bold red stalks and red veins running through the leaves, it won’t surprise you to learn they’re considered the same species (Beta vulgaris), but different sub-species. (No need to worry about pink urine from eating chard, though!) Chard comes in the same bright red color as beets, but you may also see stalks and ribs that are yellow, pink, or white. Chard is also known as silverbeet or mangold. The word “chard” comes from the French carde and the Latin carduus, meaning artichoke thistle or cardoon, including the artichoke. It’s less clear where the “Swiss” part originated, since this plant is native to the Mediterranean, not Switzerland. (It may have first been formally described by a Swiss botanist.)

Like other greens, chard is rich in vitamin K1 and folate, and it’s also a good source of vitamin C, magnesium, potassium, and manganese. It’s high in fiber, and its calorie content is almost negligible—just 19 calories for around 3.5 ounces. (Not surprising, considering they’re about 93 percent water!) Some of the minerals may be lost to the cooking water when chard is boiled, which is unfortunate, because boiling is an often-recommended cooking method for chard. This is due to chard’s high oxalate content, as some of the oxalic acid may be reduced when the vegetable is boiled. Chard is typically included on lists of high oxalate foods, particularly for individuals with recurrent kidney stones. While some individuals may need to limit their intake of these foods, a reasonable amount of chard is fine for most people. (Some people confuse chard and rhubarb, as their red stalks do look similar. Rhubarb leaves are far higher in oxalate than chard’s are.)

Chard can be very bitter, so it is sometimes paired with sweeter ingredients to help take some of the edge off. Raisins are a classic pairing with chard, such as in Swiss chard and golden raisins, or Spanish-style Swiss chard with raisins and pine nuts. Chard is often paired with nuts, such as rainbow chard with hazelnuts, and Swiss chard salad with toasted walnuts. For anyone looking to change up their creamed spinach, how about creamy chard? Like any leafy green, chard is great for low-carb, Paleo, vegetarian, and vegan diets. It pairs well with green herbs (like in these Swiss chard fritters), and is a great accompaniment to meat or poultry, like in rainbow chard and chicken stir-fry.

The attractive colors of chard are more than just pleasing to the eye. The different colored cultivars contain different types of betalains—phytochemicals that may help support phase II detoxification (reddish-purple betacyanin pigments in the red chard and yellow betaxanthin in the yellow). Like many other vegetables, chard is rich in antioxidants. The antioxidant activity and variety of phenolic compounds differs between the leaves and the stems, which is a good reason to eat both. The leaves are typically sautéed, and the stems can be cooked the same way, but don’t be surprised if you ever see both parts on a pizza! (Use a gluten-free crust if you prefer.)

 

Sources

  1. Young-Hee Pyo et al., Antioxidant activity and phenolic compounds of Swiss chard (Beta vulgaris subspecies cycla) extracts. Food Chemistry, Vol 85, Issue 1, March 2004, Pages 19-26.
  2. The World’s Healthiest Foods, Swiss chard. http://www.whfoods.com/genpage.php/genpage.php?tname=foodspice&dbid=16 (Accessed September 12, 2016).
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CoQ10 is a powerful antioxidant that provides protective properties against oxidative stress. While previous research that looked at CoQ10 supplementation on biomarkers of glucose metabolism, lipids, inflammation, and oxidative stress has been inconsistent, a recent study sheds new light on this subject.

According to this study, which was published last month in the Journal of the American College of Nutrition, researchers demonstrated beneficial effects of CoQ10 on glucose metabolism, decreased plasma malondialdehyde (MDA), and advanced glycation end products (AGEs) in individuals with diabetes.

This study was a randomized double-blinded placebo-controlled study with 50 individuals from 40-85 years of age with diabetic nephropathy. Participants were randomly assigned to take either 100 mg a day of CoQ10 or placebo for 12 weeks. Laboratory assessments were conducted at baseline and after 12 weeks (at the end of the study).

After three months of CoQ10 supplementation, there were significant decreases in serum insulin levels, homeostatic model of assessment for insulin resistance (HOMA-IR), homeostatic model assessment for B-cell function (HOMA-B), quantitative insulin sensitivity check index (QUICKI), HbA1c, MDA and AGEs. CoQ10 supplementation did not alter fasting blood glucose levels or lipid concentrations.

Inositol is another nutrient that should be considered with insulin resistance. Inositol acts as second messenger, which regulates several hormones such as thyroid stimulating hormone and insulin. Studies have shown that an inositol deficiency is common in patients with this condition. There appears to be a reduced ability to process, metabolize, and effectively use inositol from foods, this being a distinctive characteristic feature of insulin resistance. As a result, the nutritional requirements of these patients may not be met by a simple change in the diet and, therefore, inositol should be viewed as a conditionally essential nutrient for these individuals.

By Michael Jurgelewicz, DC, DACBN, DCBCN, CNS

 

Source: Gholnari T, Aghadavod E, et al. The Effects of Coenzyme Q10 Supplementation on Glucose Metabolism, Lipid Profiles, Inflammation, and Oxidative Stress in Patients with Diabetic Nephropathy: A Randomized, Double-Blind, Placebo-Controlled Trial. J Am Coll Nutr. 2018 Mar-Apr;37(3):188-193. doi: 10.1080/07315724.2017.1386140.

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Nutritionists and health advocates have been promoting the consumption of fish and seafood for decades. As the richest and most direct source of anti-inflammatory, brain-boosting omega-3 fatty acids, this food group needed to be embraced as a regular part of the American diet. Omega-3 fatty acids have become a critical tool in our rising battle against chronic diseases, most of which is rooted in systemic inflammation.

Many Americans have been raised to prefer beef and chicken while turning up their noses to fish and seafood. Therefore, in an attempt to introduce the traditional palate to a healthier fare, some health practitioners have not focused on giving clients “best practices” for seafood selection. Hence, these individuals may choose that which is the least expensive, the most widely available, and mild-tasting; namely, farmed tilapia. Tilapia not only remains the top choice of fish for most Americans, but also is highly utilized in the restaurant industry.

While we may try to rationalize the practice of consuming farmed tilapia, by calling it a stepping stone toward healthier options such as salmon, current research is arguing against such reasoning. Previous research from Wake Forest School of Medicine warns us of the dangerously high omega-6 to omega-3 ratios found in farmed tilapia, promoting inflammation and contributing to America’s top cause of mortality – heart disease. In fact, media headlines continue to declare tilapia to be more detrimental than bacon. This claim originates from research that discovered farmed tilapia contained more long-chain omega-6 fatty acids than commercially raised hamburger and bacon, and even doughnuts.

Media reports which have refuted the purported health benefits of tilapia have most likely contributed to the slight decrease in the United States’ demand for farmed tilapia since 2017; however, the US still receives 70 percent of the total international imports of farmed tilapia, primarily from China. Clearly, we are still consuming large amounts of farmed tilapia.

After initial studies of the fatty acid content of farmed tilapia were published, researchers began making proposals to supplement the diet of farmed tilapia with linseed oil, based on controlled studies. But even if supplemental linseed oil improves the omega ratios, are there other health-damaging effects of consuming farmed tilapia?

According to the Monterey Bay Aquarium (MBA) Seafood Watch China report, there are several problems with the United State’s primary source of tilapia. The report admits that “disease-related mortalities are now frequent” in response to high-intensity feeding that includes fishmeal to increase growth rates, and the presence of accumulated waste material which is not well-regulated (nor are the current regulations enforced). Furthermore, there is evidence that banned or illegal chemicals including antibiotics, malachite green (a parasiticide), and methyl testosterone hormones are still used in China fisheries. Many of these chemicals were banned in 2002, but reports indicate a lack of enforced regulation. Despite these concerns, the MBA Seafood Watch still rates farmed tilapia from China as a good alternative to the best choices of seafood.

Imported, farmed tilapia is also likely to contribute to heavy metal toxicities. In a study by the Bulletin of Environmental Contamination and Toxicology, the metal content in the tissues of tilapia raised in fisheries located near industrial parks (especially in south China where natural wind patterns cause contaminants to accumulate) proved to be dangerous to consumer’s health. Results showed significant concentrations of Mn, Ni, Pb, Zn, Cd, Tl, and As which placed the health risk in the 95th percentile of the hazard quotient and excess lifetime cancer risk for consumers.

Fish and seafood is still a superb dietary choice for obtaining healthy omega-3 fatty acids, but as practitioners, we can no longer give vague guidelines for this specific food group. Instead, we must warn consumers of the potential dangers of common choices such as farmed tilapia and instead, direct them to purchase superior selections such as the omega-3 powerhouse, wild salmon.

 

Related Products: Detox Antiox™, Pure PaleoCleanse Plus™ Detox Program, VegeCleanse Plus™ Day Detox Program, Detox Support Packets

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