Figure of mouse brain tissue from the substantia nigra; cells that are stained are dopamine producing.

Parkinson’s disease (PD) is a neurodegenerative disease, which means that the damage in the brain begins several decades before the symptoms appear. In PD, approximately 60% of a specific cell type in the brain dies before symptoms appear. The cells that die are dopamine-producing cells. Dopamine is a neurotransmitter, which is a chemical in the brain that help cells communicate with each other. Dopamine cells within the substantia nigra, an area of the brain, die in PD. In the figure above you can see dopamine-producing cells. PD was first described in 1817 by James Parkinson, and although the exact cause of PD still remains unknown, researchers and clinicians know that changes in our DNA play an important role. There is also an environmental component–for example, exposure to herbicides like paraquat induce PD in people. Another example of an environmental contributor is nutrition. 

Nutrition, specifically B-vitamins, have been implicated in the onset and progression of PD. Folic acid is an example of a B-vitamin, and it is well known for its role in preventing neural tube defects during early brain development. Additionally, folic acid also helps to lower levels of a chemical called homocysteine. High levels of homocysteine are present in PD patients who take levodopa (L-DOPA), a pharmaceutical drug that helps replenish dopamine in the brain. The breakdown of L-DOPA in the body requires methyl groups generated from folic acid, and this in turn increases levels of homocysteine.

Methylenetetrahydrofolate reductase (MTHFR) is a protein that breaks down folic acid to generate methyl groups, and people with reduced levels of this protein are reportedly more affected by PD. In a recent research study from our group we use a mouse model with reduced levels of MTHFR to study how the paraquat model of PD impacts onset and progression.

Our study found that reduced levels of MTHFR result in motor impairments in PD mice, and these impairments are characteristic of PD. Additionally, the PD mice were sick and had higher levels of inflammation in the substantia nigra. There were also high levels of oxidative stress, which is an imbalance of reactive oxygen and antioxidant production within a brain region closely connected to the substantia nigra. Higher levels of oxidative stress have been implicated in several neurodegenerative diseases. In terms of targeting oxidative stress through pharmaceuticals, there has not been much progress. Food stuffs such as red wine, green tea, and blueberries have been reported ro reduce levels of oxidative stress through their antioxidant properties, but more investigation is required.  

Nutrition is an important aspect of health. It is well documented that not all older adults absorb as many nutrients compared to their younger counterparts due to several factors, one being inflammation in the stomach. These recent research findings presented in this blog along with others suggest that adequate nutrition should be a component of health care for patients with PD.

Review published in Advances in Nutrition finds increasing dairy may be an effective strategy to combat sarcopenia.

As we age, we tend to lose muscle mass and muscle strength.  This progressive muscle loss, known as sarcopenia, can begin as early as our forties, depending on several factors, including diet and physical activity.

Sarcopenia has been linked to an increased risk of physical disability, depression, debilitating falls, and death.  With the aging of the population, the incidence of sarcopenia is expected to dramatically rise in the coming decades: more than 200 million cases are projected by 2050.  As such, sarcopenia is a major global public health challenge.

Researchers have learned that diet and lifestyle play a major role in both the onset and progression of sarcopenia.  Studies have shown, for example, that protein supplementation combined with resistance exercise can reverse the effects of sarcopenia among older adults.

Dairy products, which are good sources of high-quality protein, may be particularly well suited for combating sarcopenia. They are relatively affordable and generally available throughout the world.  Moreover, they typically require no cooking or only minimal preparation compared with other protein-rich foods such as lean meat, poultry, fish, and eggs. This makes dairy a highly practical option for older adults who need to increase their protein intake.

Recently published in Advances in Nutrition, “The Impact of Dairy Protein Intake on Muscle Mass, Muscle Strength, and Physical Performance in Middle-Aged to Older Adults with or without Existing Sarcopenia: A Systematic Review and Meta-Analysis” examines the current body of evidence in order to assess the impact dairy protein may have on preventing or reversing sarcopenia.  In particular, the authors looked at how increased dairy intake affected arm and leg muscle mass and strength.

To conduct their research, the authors performed a thorough search of randomized controlled trial studies. Their search led them to 14 relevant studies involving 1424 participants between the ages of 61 and 81 years. The results of their analysis of these studies indicate that 14 to 40 grams of dairy protein per day led to a “significant favorable effect of dairy protein” on arm and leg muscle mass.  Moreover, study participants were generally able to easily tolerate increased dairy intake without any adverse effects.

In conclusion, the authors noted, “Although future high-quality research is required to establish the optimal type of dairy protein, the present systematic review provides evidence of the beneficial effect of dairy protein as a potential nutrition strategy to improve appendicular muscle mass in middle-aged and older adults.”

We are all susceptible to sarcopenia as we grow older.  Increased dairy may be an effective strategy to prevent the onset or progression of sarcopenia.  You should, however, consult a health care professional before making major dietary changes, as individual needs and tolerances to dairy vary.

A healthy, balanced diet is important for overall good health, but certain nutrients, such as protein, calcium, vitamin D, potassium, phosphorus, magnesium, and zinc, are particularly important for healthy bones.

Inadequate intakes of these nutrients increase the risk of bone loss and subsequent risk of osteoporosis, a condition characterized by low bone mineral density. Because dairy foods provide more of these bone-benefiting nutrients per calorie than any other food, consumption of dairy foods has been shown to be positively related to bone mineral density and reduced bone loss over time among a narrow sample of non-Hispanic whites. Although Puerto Rican adults (the second-highest represented subgroup of Hispanics in the United States) have a higher prevalence of osteoporosis and vitamin D deficiency than non-Hispanic whites, the impact of dietary choices on bone health in this population is poorly understood. Findings from a recent study conducted by Drs. Kelsey Mangano, Katherine Tucker, and Sabrina Noel (University of Massachusetts-Lowell) and published in the January 2019 issue of The Journal of Nutrition, reveal a unique dietary pattern that may detrimentally affect bone health.

To test their hypothesis, a total of 904 participants from the Boston Puerto Rican Osteoporosis Study provided diet information using a culturally tailored food-frequency questionnaire. For this study, dairy food groups included milk, yogurt, fluid dairy (milk + yogurt), cheese, cream and dessert dairy. Bone mineral density was measured using dual-energy X-ray absorptiometry, and vitamin D status was defined as sufficient or insufficient using a standard blood test.

The researchers found that higher intakes of modified dairy (milk + yogurt + cheese) and milk alone were significantly associated with higher bone mineral density. However, when compared by vitamin D status, total dairy, fluid dairy (milk + yogurt), and milk intake were significantly related to higher bone mineral density only among those with vitamin D sufficiency. Calcium and vitamin D intakes from all foods were lower than in the Dietary Guidelines, whereas protein intakes were higher compared with other adult populations. The scientists concluded that this unique dietary pattern may detrimentally affect bone health, because dietary protein intakes appear to be protective only under conditions of adequate calcium intake. Potential interventions to improve bone health should include dairy products in combination with public health messages to improve vitamin D sufficiency. Future studies should confirm these findings as well as assess culturally acceptable strategies to improve bone health among Hispanic adults.

Reference Mangano KM, Noel SE, Sahni S, Tucker KL. Higher Dairy Intakes Are Associated with Higher Bone Mineral Density among Adults with Sufficient Vitamin D Status: Results from the Boston Puerto Rican Osteoporosis Study. Journal of Nutrition. 2019; In Press.

https://doi.org/10.1093/jn/nxy234

A logical start when we think about nutrition is the mouth. The mouth is the first point of entry for all nutrients, in the form of the food we consume. Oral health and periodontal disease and their connection to nutrition run bi-directionally, where several studies have shown associations between individual micronutrients and periodontitis [1, 2]. Additional associations have been found between cumulative histories of oral problems including untreated caries, poor oral health, dental pain, restorations, extractions, use of prosthetics and food insecurity [3].

Periodontitis is defined as an inflammatory disease of the supportive tissues of the teeth caused by microorganisms which result in progressive destruction of periodontal ligaments and alveolar bone [4]. Periodontitis impacts 40-90% of the world’s population and is one of the most prevalent epidemics globally. Several micronutrients also impact periodontal health and include vitamin A (carotenoids, β-carotene), vitamin C (ascorbic acid), vitamin E (α-tocopherol), glutathione and melatonin [5,6]. These anti-oxidants have been shown to help overcome reactive-oxygen species mediated inflammation present in periodontal tissue which leads to periodontitis.

It is estimated that 15.8 million children under the age of 18 years in the United States live in households that are unable to access nutritious food necessary for healthy growth on a consistent basis [7]. In addition, over-nutrition in the form of childhood obesity and overweight, particularly among lower income children, is compounded by a preponderance to more cariogenic foods. A study conducted in Japan documented association between high body mass index (BMI) and increased risk of periodontal disease among young adults [8]. An abundance of fast food, poor quality, high sugar and simple carbohydrate-based diets in lower income neighborhoods predispose children to the development of plaque, dental decay and caries [9, 10]. Inadequate consumption of fruits and vegetables deprive children of the nutrients they need for healthy growth and development [10]. Proper oral health care started at a young age is essential to ensure good nutrition and oral hygiene into adolescence and adulthood.

Pregnant women are more prone to periodontitis, gingivitis and gingival hyperplasia. Increased secretion of estrogen during pregnancy has also been linked to periodontal disease during pregnancy [11]. Periodontal disease both during preconception and in pregnancy has been linked to adverse outcomes including premature birth, preeclampsia, gestational diabetes, fetal loss, small for gestational age babies [12]. Antioxidant rich foods consumed during pregnancy, in addition to diets high in fiber and low in refined sugar are important to prevent periodontal disease. Improved oral hygiene is also essential.

In America, life spans have increased by upwards of 30 years in the last century. It is estimated that by 2050, people will live to an average age of 100 [13]. The elderly, in addition to children and pregnant women, are also susceptible to the impacts of nutrition on oral health. Among this age group, compromised oral health care, due to age-related factors such as tooth loss, use of oral prosthetics, a lack of appetite and mastication ability, in addition to altered taste and gastrointestinal conditions, are important concerns. An inability to consume certain foods due to difficulties with chewing and swallowing can compound food insecurity [14, 15]. Oral care in the elderly and customized nutrition to account for their complex needs is essential to ensure good quality of life.

The link between good oral health and nutrition is undeniable and complex. It is time for more concerted efforts to be made to link the two interconnected areas of health, across the lifespan. Increased efforts to educate oral health providers on the importance of nutrition education, in addition to ensuring proper nutrition security for at risk groups, will ensure healthy bodies and wide toothy smiles!

 

References:

[1] Dommisch, Kuzmanova, Jonsson, Grant & Chapple. (2018). Effect of micronutrient malnutrition on periodontal disease and periodontal therapy. Periodontology 2000, 78, 129-153.

[2] Najeeb, S., Zafar, M.S., Khurshid, Z., Zohaib, S., & Almas, K. (2016). The role of nutrition in periodontal health: An update. Nutrients, 8, 530.

[3] Santin, G.C., Martins, C.C., Pordeus, I.A., & Ferreira, F.M. (2014). Food insecurity and oral health: A systematic review. Pesquisa Brasileira em Odontopediatria e Clinica Integrada, 144, 335-246.

[4] Newman, G.M., Takei, H.H., Klokkevol, R.P., Carranza, A.F. (2012). Carranza’s clinical periodontology. Classification of diseases and conditions affecting the periodontium. In Carranza’s Clinical Periodontology, 12th ed.; Michael, G.N., Henry, H.T., Perry, R.K., Fermin, A.C., Eds.; Elsevier: Amsterdam, The Netherlands, pp. 45-67.

[5] Garcia, J.J., Reiter, R.J., Guerrero, J.M., Escames, G., Yu, B.P., Oh, C.S., & Munoz-Hoyos, A. (1997). Melatonin prevents changes in microsomal membrane fluidity during induced lipid peroxidation. FEBS Letters, 408, 297-300.

[6] Najeeb, S., Khurshid, Z., Zohaib, S., & Zafar, M.S. (2016). Therapeutic potential of melatonin in oral medicine and periodontology. Kaohsiung Journal of Medical Sciences, 32, 391-396.

[7] Coleman-Jensen A, Gregory C, Singh A. (2014). Household Food Security in the United States in 2013. USDA ERS.

[8] Ekuni., D., Yamamoto, T., Koyama, R., Tsuneishi, M., Naito, K., & Tobe, K. (2008). Relationship between body mass index and periodontitis in young Japanese adults. Journal of Periodontitis Research, 43, 417-421.

[9] Moynihan P, Petersen PE. (2004). Diet, nutrition and the prevention of dental diseases. Public Health Nutrition, 7(1A):201-226.  Accessed 7/7/2015 at https://www.who.int/nutrition/publications/public_health_nut7.pdf.

[10] Edgar, W. (1993). Extrinsic and instinsic sugars: A review of recent UK recommendations on diet and caries. Caries Research, 27, 64-67.

[11] Hemalatha, V., Manigandan, T., Sarumathi, T., Aasthi Nisha, V., & Amudhan, A. (2013). Dental considerations in pregnancy – A critical review on oral care. Journal of Clinical Diagnostics Research, 7, 948.

[12] Ziegler, J., & Mobley, C.C. (2014). Pregnancy, child nutrition and oral health. Chapter 2: In Nutrition and Oral Medicine; Touger-Decker R., Mobley, C., & Epstein, J.B., Eds. Springer Science+Business Media, New York, pp. 19-37.

[13] Ham-Chande, R., (2005). Shapes and limits of longevity in Mexico. In proceedings of the living to 100 and beyond symposium, Orlando, FL, USA, 12-14 January 2005.

[14] Sheiham, A., & Steele, J. (2001). Does the condition of the mouth and teeth affect the ability to eat certain foods, nutrient and dietary intake and nutritional status amongst older people? Public Health Nutrition, 4, 797-803.

[15] Brodeur, J., Laurin, D., Vallee, R.,&  Lachapelle, D. (1993). Nutrient intake and gastrointestinal disorders related to masticatory performance in the edentulous elderly. Journal of Prosthetics and Dentistry, 70, 468-473.

According to the United Nations the aging population is growing and by 2050 the number of people aged 60 years old will reach 2 billion worldwide. With the aging population the prevalence of age-related disease is predicted to increase. An example of an age-related disease is neurodegeneration.  Dementia can be a result of several pathologies including increased levels of Lewy bodies (abnormal aggregates of protein in nerve cells), as seen in Parkinson’s disease.

Cerebrovascular disease is the second most common cause of dementia and is a result of  changes in blood flow to or within the brain. Blood flow in the brain can change because of hypertension, diabetes, smoking, and hypercholesterolemia. Patients with cerebrovascular disease experience cognitive impairment, specifically when trying to remember things or plan events/trips. It is important to note that symptoms can vary from patient to patient. A type of cerebrovascular disease is vascular cognitive impairment (VCI).

Nutrition is a modifiable risk factor for diseases of aging. As people age their ability to absorb nutrients from their diet decreases.  Several studies have reported that changes in B-vitamin absorption may play a role in the onset and progression of dementia. Additionally, a study by researchers in the United Kingdom shows that B-vitamin supplementation reduced brain volume loss in areas associated with cognitive decline. A recent international consensus statement from leaders in the field suggests that deficiencies in B-vitamin metabolism should be considered when screening dementia patients. My research using model organisms has tried to understand the disease processes associated with dementia.

Using a mouse model of VCI we have reported that deficiencies in folic acid, either dietary or genetic affect the onset and progression of VCI. Using the Morris water maze task we report that mice with VCI and folate deficiency performed significantly worse compared to controls. We assessed changes in the brain using MRI and interestingly found that folate deficiency changed the vasculature in the brains of mice with VCI. Because of either a genetic or dietary folate deficiency all the mice had increased levels of homocysteine.

Our results suggest that it is not elevated levels of homocysteine making the brain more vulnerable to damage, but the deficiency in folic acid, either dietary or genetic, that changes the brain. In the cell folic acid is involved in DNA synthesis and repair as well as methylation. These are vital functions for normal cell function. Therefore, reduced levels of folate may be changing the cells in the brain and making them more vulnerable to certain types of damage. We think that high levels of homocysteine may just be an indication of some deficiency (e.g. reduced dietary intake of folic acid). Maintaining normal levels of homocysteine are needed, since studies in humans have shown that elevated levels of homocysteine are a risk factor for neurodegenerative diseases and that reducing them is beneficial.

 

The popularity of the essential polyunsaturated omega-3 fatty acids (O3FA) is on the rise. In 2017, O3FA achieved a spot on the top 20 foods and ingredients list that Americans are adding to their diets (The Hartman Group). In addition, the global fish oil market is expected to reach a whopping 4.08 billion dollars in the next four years!  The proposed health benefits are likely the driving force behind the increasing demand.

Despite their booming popularity, a large percentage of adults are not meeting the O3FA recommended intake. There are three primary O3FAs with distinct characteristics: alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Although commonly grouped under the umbrella term O3FAs, are all O3FAs created equal?

Unique Characteristics of O3FAs

Omega-3 fatty acids cannot be sufficiently produced in the body earning them the title of “essential fatty acids.” The plant-derived omega-3, ALA, is the parent precursor to EPA and DHA. Unfortunately, the conversion rate in our bodies is very low.  It is important to realize that in the process of metabolizing ALA to EPA and DHA, a series of anti-inflammatory markers are produced (leukotrienes, prostaglandins and thromboxane). As these anti-inflammatory metabolites are beneficial, direct EPA and DHA consumption is needed to meet bodily requirements.

Independent and Complementary Health Benefits

The majority of current research focuses on the health benefits of marine fatty acids.  DHA and EPA consumption portray an array of shared and complementary benefits related to the treatment of cardiovascular disease, depression diabetes, sleep disorders and more. DHA is more significantly associated with decreases in resting heart rate, blood pressure and with improvements in cellular membrane health due to its additional double bond and longer carbon chain. Increased cellular levels of EPA have been shown to benefit coronary heart disease, hypertension and to decrease inflammation. EPA and DHA are both associated with reduced gene expression related to fatty acid metabolism, reduced inflammation and oxidative stress.

Specific supplementation of ALA is not consistently associated with cardiovascular health. Although plant-derived ALA can be easily substituted in for excess omega-6 fatty acids (O6FAs). Research has shown that by reducing the O3FA:O6FA ratio, you can decrease bodily inflammation, increase anti-inflammatory markers and more efficiently utilize EPA and DHA.

An ALA, EPA and DHA-Rich Diet

The 2015-2020 Dietary Guidelines for Americans recommends that healthy adults consume at least 8 ounces of a variety of non-fried fatty seafood per week. For EPA and DHA requirements, the American Heart Association recommends fatty marine sources containing 500 mg or more of EPA and DHA per 3oz cooked serving (e.g., salmon and tuna).   ALA is the most commonly consumed O3FA in the Western diet as it is found in plant-based foods (e.g., dark green leafy vegetables, walnuts, canola oil, flax seed). Unlike EPA and DHA, an Adequate Intake (AI) level is established at 1.6 g/day and 1.1 g/day for men and women respectively.

The Final Verdict 

The wide range of benefits stemming from marine O3FAs indicates the importance of regular consumption of fatty seafood and EPA and DHA-containing products.  The incorporation of plant-derived ALA may serve more importantly as a substitute for omega-6 fatty acids to reduce bodily inflammation, decrease the high O3FA:O6FA ratio typically observed in the Western diet, and to help elevate EPA and DHA levels in the body. EPA and DHA may be featured as the health promoting “dynamic duo,” but ALA is still invited to the party!

 

References

1.         Yanni Papanikolaou JB, Carroll Reider and Victor L Fulgoni. U.S. adults are not meeting recommended levels for fish and omega-3 fatty acid intake: results of an analysis using observational data from NHANES 2003–2008. Nutrition Journal 2014.

2.         Harris WS, Mozaffarian D, Lefevre M, Toner CD, Colombo J, Cunnane SC, Holden JM, Klurfeld DM, Morris MC, Whelan J. Towards establishing dietary reference intakes for eicosapentaenoic and docosahexaenoic acids. J Nutr 2009;139(4):804S-19S. doi: 10.3945/jn.108.101329.

3.         Frits A. J. Muskiet MRF, Anne Schaafsma, E. Rudy Boersma and Michael A. Crawford. Is Docosahexaenoic Acid (DHA) Essential? Lessons from DHA Status Regulation, Our Ancient Diet, Epidemiology and Randomized Controlled Trials. Journal of nutrition 2004;134.

4.         Mozaffarian D, Wu JH. (n-3) fatty acids and cardiovascular health: are effects of EPA and DHA shared or complementary? J Nutr 2012;142(3):614S-25S. doi: 10.3945/jn.111.149633.

5.         Bork CS, Veno SK, Lundbye-Christensen S, Jakobsen MU, Tjonneland A, Schmidt EB, Overvad K. Dietary Intake of Alpha-Linolenic Acid Is Not Appreciably Associated with the Risk of Ischemic Stroke among Middle-Aged Danish Men and Women. J Nutr 2018. doi: 10.1093/jn/nxy056.

6.         Evangeline Mantzioris MJJ, Robert A Gibson and Leslie G Cleland Differences exist in the relationships between dietary linoleic and alpha-linolenic acids and their respective long-chain metabolites. Am J Clin Nutr 1995;61:320-4.

7.         Agriculture. USDoHaHSaUSDo. 2015 – 2020 Dietary Guidelines for Americans. 8th Edition. December 2015.

By: Nafisa M. Jadavji, PhD

 

A stroke occurs when there is reduced blood flow to the brain. Blood carries oxygen and glucose to cells in the brain. When there are reduced levels of blood, these cells start to die. Since the brain controls behavior, this cell death leads to impairments in function. The impairments are dependent on where the stroke happens in the brain. There are two main types of stroke: hemorrhagic and ischemic. For this blog, I will be focusing on ischemic stroke which is a result of blockage in a blood vessel. Currently, stroke typically affects older individuals and the global population is aging according to the United Nations. Additionally, older individuals also lose their ability to absorb all the vitamins and nutrients they require from their diet as they age.

Nutrition is a modifiable risk factor for diseases of aging. For example, B-vitamin absorption decreases as individuals age. B-vitamins play a major role in reducing levels of homocysteine, a non-protein amino acid. High levels of homocysteine have been associated with increased risk to develop cardiovascular diseases, such as stroke. Supplementation with B-vitamins has been reported to have positive effects on brain health.

A study by researchers in Oxford University and University of Oslo has shown that B-vitamin supplementation in the elderly within the United Kingdom reduced age-related brain atrophy after 2 years of supplementation. Furthermore, another study by the same group reported that B-vitamin supplementation reduced cerebral atrophy in areas vulnerable to Alzheimer’s disease.

More recently, a group from China reported that folic acid supplementation in combination with Enalapril, used to treat heart disease, reduced the risk of stroke by 21% in patients that were hypertensive.

Within the aging population, B-vitamin supplementation has been reported to have positive effects on brain health. The elderly are more prone to ischemic stroke, but the mechanisms through which this benefit is accomplished are not well understood.

A recent study investigating the role of B-vitamin supplementation on ischemic stroke was published in the Neurobiology of Disease. This study tried to examine the mechanisms of how supplementation improved brain function. A group of wildtype males were put on a folic acid deficient diet (0.2 mg/kg) prior to ischemic damage to increase levels of homocysteine and another group of mice were put on a control diet (2mg/kg folic acid). After ischemic damage to the sensorimotor cortex, FADD mice were put on a supplemented diet, where levels of folic acid, riboflavin, vitamin B12, and choline were increased. Animals were maintained on the diets for 4-weeks after which motor function was assessed.  Researchers found that supplemented diet mice performed better on motor tasks compared to CD mice with ischemic damage. In the brain tissue, increased levels of plasticity and antioxidant activity were reported.

Combination therapies for stroke-affected patients are thought to be most effective. A pharmaceutical in combination with a lifestyle change, such as increased exercise may be beneficial for stroke-affected patients. This data suggests that nutrition may also be a viable option to prevent or attenuate ischemic damage.

 

 

Omega-3 fatty acids have been long touted for their cardiovascular benefits. But many research studies strongly suggest that these fatty acids exert improvements well beyond those related to heart health.

 

Omega-3 fatty acids and/or fish oil supplements (the latter being a rich source of omega-3s) have been administered to those with cancer, heart disease, rheumatoid arthritis, and psychiatric disorders (i.e. schizophrenia and major depressive disorder) with resultant improvements in disease-specific outcomes and body composition (read: more and/or better quality of muscle) (1, 2). The supplement also has essentially no side effects, aside from the occasional lingering fishy after-taste. It’s thought that these beneficial effects are due to omega-3’s inhibition of numerous pro-inflammatory pathways.

So is there a place for these supplements in healthy populations? Say, exercising older adults? This is exactly what Mariasole Da Boit and a group of colleagues investigated in a randomized, double-blind placebo controlled trial published in the American Journal of Clinical Nutrition earlier this year (3). Fifty men and women (age 70.6 ± 4.5) participated in a resistance exercise training program for lower limbs twice weekly for 18 weeks. All were randomized to 3g fish oil/day or placebo (3g safflower oil/day). In women, maximal isometric torque (static contraction) and muscle quality defined by torque per unit of muscle cross-sectional area improved more in the fish oil group, independent of muscle mass changes; no differences were observed in men. Plasma triglycerides decreased in both sexes, while maximal isokinetic torque (moving contraction), 4-minute walk test, chair-rise time, muscle size, and muscle fat did not differ. The authors speculate that omega-3 improves neuromuscular function and/or enhances the contractile properties of type II (fast-twitch) muscle fibers. Some findings suggest that older women do not increase muscle strength to the same degree as older men; thus women could undergo a more profound response to resistance training since there is a greater capacity for muscular improvement.

While this is only one study and the mechanisms behind the results are somewhat speculative, the results are promising. With forthcoming research, omega-3 fatty acid supplements might become an evidence-based recommendation for healthy community-dwelling older adults and many clinical populations.

  1. Lee S, Gura KM, Kim S, Arsenault DA, Bistrian BR, Puder M. Current clinical application of omega-6 and omega-3 fatty acids. Nutrition in Clinical Practice 2006; 21(4):323-41
  2. Murphy RA, Mourtzakis M, Chu QS, Baracos VE, Reiman T, Mazurak VC. Nutritional intervention with fish oil provides a benefit over standard of care for weight and skeletal muscle mass in patients with nonsmall cell lung cancer receiving chemotherapy. Cancer 2011;117(8):1775-82.
  3. Da Boit , Sibson R, Sivasubramaniam S, Meakin JR, Greig CA, Aspden RM, et al. Sex differences in the effect of fish-oil supplementation on the adaptiveresponse to resistance exercise training in older people: a randomized controlled trial. American Journal of Clinical Nutrition 2017; 105:151-8

Many dangerous fad diets exist that purport to treat diseases such as cancer by manipulating the pH of blood with different foods. While there is no good evidence that acidic foods alter the body’s pH and promote disease, the hypothesis that “dietary acid load” relates to disease should not be completely dismissed. The kidney serves to regulate blood pH, but if kidney function declines and other tissues catabolize to maintain pH, then it is very plausible that manipulating the diet to reduce the acid load could spare tissues and improve outcomes in chronic kidney disease (CKD). After all, for example, the metabolism of amino acids yields hydrogen ions, whereas fruits and vegetables contain organic salts that generally reduce acid load when metabolized. Recently, a growing number of human studies that manipulate diet acid load using fruits and vegetables and sodium bicarbonate support this hypothesis. Let’s take a look at some of them.

The first randomized controlled trial on bicarbonate supplementation and CKD progression was published in 2009 by de Brito-Ashurst and colleagues. Bicarbonate is produced by the kidneys and serves to neutralize acid. Supplementation of bicarbonate for 1 year in CKD patients slowed the progression of kidney disease as suggested by creatinine clearance and reduced the need for dialysis. The next year, in 2010, a 5-year trial was published by Donald Wesson’s group that found a slowed kidney decline as measured by estimated glomerular filtration rate (eGFR) with bicarbonate supplementation. Several subsequent studies by his group have used bicarbonate or fruits and vegetables to achieve beneficial outcomes. Goraya et al. gave oral bicarbonate or enough fruits and vegetables that were estimated to reduce dietary acid load by 50% to CKD patients for 30 days and also observed a slowed reduction in eGFR in patients at moderate, but not mild, stages of the disease. In patients with more advanced stages of CKD, one year of bicarbonate or fruits and vegetables did not slow the decrease in eGFR, though several urinary markers of kidney injury were reduced. Their most recent trial tested if kidney function might be preserved through a reduction in angiotensin II in moderate stage CKD patients. Three years of bicarbonate or increased fruits and vegetables lessened the decline in eGFR and resulted in a corresponding decrease in the marker angiotensin II. Other studies using bicarbonate from six months to two years have provided strong evidence that reducing acid load consistently slows the decline of eGFR, and improves markers of bone health and muscle function.

Each of the studies described provided fruits and vegetables to patients free of charge to increase adherence. It will be important to test if adherence can be maintained through education alone. Additionally, it may be that “prescribing” fruits and vegetables is effective at improving outcomes and reducing health care costs more so than bicarbonate since they also reduce blood pressure. While “alkaline diets” in general should be viewed skeptically, there is accumulating evidence that fruits and vegetables as dietary alkali do indeed help in kidney disease.

By Caitlin Dow, PhD

The most recent data from the CDC indicates that approximately 35% of American adults have obesity (1). In order to reduce obesity prevalence, a popular notion is that people with obesity just need to “eat less and move more.” Indeed, many public health programs use this concept as their primary approach for combating obesity. While eating less and moving more may help prevent obesity or result in successful, sustained weight loss in individuals who are simply overweight (but not yet obese), ongoing research indicates that these simple lifestyle changes will do very little in the face of prolonged obesity (2).

If you look at any weight loss study, you will most assuredly find the same results, regardless of study design. The first six months are generally characterized by substantial weight loss, followed by sustained weight regain, resulting in a final weight that is negligibly lower and potentially higher than the starting weight . This “checkmark effect” or weight loss recidivism that has been reported nearly ubiquitously across diet and exercise-based weight loss trials (3) indicates that lifestyle interventions are generally not successful modalities for treating obesity.

Based on a rudimentary understanding of metabolism, the calories in/out approach should work for weight loss and weight loss maintenance. So why doesn’t it work for so many people? The answer lies in the complex network linking the environment, genetic predisposition to obesity, as well as metabolic and physiological changes. A large body of literature indicates that the brain’s reward systems are significantly dysregulated in individuals with obesity (4). In an environment that supports ease of access to highly palatable foods, the pleasurable effects of consuming said foods can override homeostatic control of intake. While some people are able to regulate intake despite the high palatability of these foods, a number of genetic mutations in the brain’s reward systems may result in overeating and obesity in many people. Furthermore, the hypersensitive reward systems that often lead to obesity can become insensitive once a state of obesity is attained. In effect, this leads to overeating to receive the same pleasure from the same foods. These dysregulated reward systems are coupled with preadipocyte expansion into mature adipocytes, allowing for increased fat storage. While this isn’t the entire story, this should shed some light on the complex interactions of dysregulated internal systems that foster the metabolic abnormalities that result in obesity. Importantly though, these impairments are typically only demonstrated once obesity has been introduced and sustained (3).

As for weight loss, when caloric restriction is initiated, the body triggers a number of systems to prevent starvation. From an evolutionary perspective, this makes sense as food sources were often unpredictable and the body adapted to conserve energy – the “feast and famine” principle. However, for most of us living in industrialized nations, famine is rare and feast is common, limiting the need for this once very necessary adaptation (though the body has not evolved to recognize the abundance of calories in our modern food supply). When we try to induce weight loss via caloric restriction, the body will reduce its resting metabolic rate to counter these advances (5). This supports the “set point theory” – the idea that the body will defend its highest-sustained weight. In fact, as weight loss increases, the drive to restore the highest bodyweight only increases (6). It’s like when you’re pulling on your dog’s leash to get him into the vet and he plants his feet firmly and resists with all his might. Ultimately his strength pulls him out of his collar and sends him running in the opposite direction. Except here we’re talking about the human body and it’s not nearly as comical.

All of these biological adaptations that introduce, sustain, and defend obesity explain why weight loss and its maintenance is so exhaustingly difficult for so many people. As Ochner and colleagues suggest, most individuals who had obesity but lost weight simply have “obesity in remission and are biologically very different from individuals of the same age, sex, and body weight who never had obesity.” As a hypothetical scenario, imagine you are comparing two people: they weigh the same, but person A had obesity and has lost weight whereas person B has never lost weight. Person A will have to burn up to 300 calories more (or consume 300 calories fewer) than person B to maintain that weight (2). This underscores the idea that weight regain is not simply an issue of willpower and weakness.

What we need more of are studies evaluating multiple approaches to weight loss (surgeries, medications, likely in combination with lifestyle changes). What we need less of is bias from people without obesity, the media, and even healthcare providers. Indeed, “the mere recommendation to avoid calorically dense foods might be no more effective for the typical patient seeking weight reduction than would be a recommendation to avoid sharp objects for someone bleeding profusely” (2). We also need better obesity prevention approaches because, clearly, it’s biologically more feasible to prevent weight gain than to lose weight and keep it off.

References

1.Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adults obesity in the United States, 2011-2012. JAMA. 2014;311(8):806-814. doi:10.1001/jama.2014.732.

2.Ochner CN, Tsai AG, Kushner RF, Wadden TA. Treating obesity seriously: when recommendations for lifestyle change confront biological adaptations. Lancet Diabetes Endocrinol. 2015:

3.Ochner CN, Barrios DM, Lee CD, Pi-Sunyer FX. Biological mechanisms that promote weight regain following weight loss in obese humans. Physiol Behav. 2013:120:106-13. doi: 10.1016/j.physbeh.2013.07.009.

4.Kenny JP. Reward mechanisms in obesity: new insights and future directions. Neuron. 2011:69(4):664-79. doi:10.1016/j.neuron.2011.02.016

5.Grattan BJ, Connolly-Schoonen J. Addressing Weight Loss Recidivism: A Clinical Focus on Metabolic Rate and the Psychological Aspects of Obesity. ISNR Obesity. 2012. doi:10.5402/2012/567530

6.Rosenbaum M, Leibel RL. Adaptive thermogenesis in humans. Int J Obes.2010:34:S47-55. doi:10.1038/ijo.2010.184