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High Glycemic Brain Damage

December 9, 2017 Written by JP       [Font too small?]

You’ve heard the carols on the radio, seen the strings of light on your way home and surely, you haven’t escaped the ceaseless advertising typical of this time of year. Take cover! The holiday season is upon us. Thankfully, I’m not here to dazzle you with glowing reindeer or the latest, greatest stocking stuffers. Instead, as 2017 gets ready to bid farewell, I’d like to a share a few, free gifts with you all. If consistently applied, I’m confident these tokens of my appreciation can improve the quality of your health and life. So, don’t wait for the start of 2018 to turn a new page – begin right now to strengthen your body, mind and spirit.

For many, this time of year can be challenging for a number of reasons – time often becomes increasingly scarce, food choices frequently get richer and sweeter, and stress in various forms from financial to social is practically a holiday tradition. Today, I’m going to offer a simple technique to pamper your brain in the coming weeks and hopefully long after that.

A just published study in the December 2017 issue of The American Journal of Nutrition reports that “normal older adults” who eat a high-glycemic diet have 26% more cerebral amyloid – a type of protein that forms plaque that is found in the brains of those with Alzheimer’s disease. According to the National Institutes of Aging, “amyloid plaques collect between neurons and disrupt cell function”. Now, if this was only a “stand alone” study, it might be interesting, but not very consequential. However, the fact is that there is an emerging body of evidence connecting elevated blood sugar (primarily caused by a high-glycemic diet) with poorer cognitive function and health.

Before I go any further, let’s briefly establish the definition of a high-glycemic diet. The glycemic index (GI) is used to categorize foods based on the degree by which they affect blood sugar. Examples of high-glycemic foods include bread, candy, potatoes, rice and sugar-sweetened soda. Examples of low-glycemic foods are cruciferous and green leafy vegetables, beef, chicken, eggs, fish, nuts and seeds. Unsurprisingly, diets that lean heavily on high-GI foods are deemed as high-glycemic diets.

One of the most worrisome points about the study I referenced above is that it detected a sign (amyloid build up) associated with brain deterioration in a group of adults without diagnosed cognitive dysfunction. In other words, from the outside looking in, they seemed healthy. Other research adds weight to the hypothesis that diet-induced hyperglycemia may harm the brain and negatively influence cognition in cognitively-intact older adults. For instance, a 2015 study noted that “High blood glucose was related to poorer overall performance on perceptual speed as well as greater rates of decline in general cognitive ability, perceptual speed, verbal ability, and spatial ability”.

At least two other trials offer insights into the role that the glycemic index may play in hastened brain aging. One study, dating all the way back to 2003, specifically looked at the effect of low vs. high glycemic breakfasts in humans and rats. A low GI breakfast alone improved post-meal memory in humans and learning performance in their rodent counterparts. The second trial is perhaps the most disconcerting of all. In it, brain imaging was used to determine the amount of gray and white matter volume in the brains of 209 “healthy children”. After analyzing the brain images and diets of the children, it was determined that those who commonly ate lower-GI breakfasts had “significantly larger gray matter … and white matter volumes of several regions”. The authors of the study concluded that a lower-GI diet may be “important for brain maturation during childhood and adolescence”.

The link between high-GI carbohydrates, erratic blood sugar and memory dysfunction is now widely accepted when referring to type 2 diabetics. I believe in the near future, a very similar attitude will be adopted with respect to non-diabetics as well – of all ages. But, why wait for an official pronouncement when it’s already quite clear that maintaining stable blood sugar via a nutrient-dense, low-glycemic diet can only benefit your brain (and your body)?

Bonus Gift! As you may already know, I have a small collection of low-glycemic recipes on my site. But, if you’re looking for some additional inspiration, I highly recommend you visit Elena Amsterdam’s recipe collection. Her creations are consistently delicious, health promoting and inventive.

Note: Please check out the “Comments & Updates” section of this blog – at the bottom of the page. You can find the latest research about this topic there!

To learn more about the studies referenced in today’s column, please click on the following links:

Study 1 - A High-Glycemic Diet is Associated with Cerebral Amyloid Burden (link)

Study 2 - Blood Glucose, Diet-Based Glycemic Load and Cognitive Aging (link)

Study 3 – The Delivery Rate of Dietary Carbohydrates Affects Cognitive(link)

Study 4 - Breakfast Staple Types Affect Brain Gray Matter Volume and … (link)

Study 5 - Carbohydrate-Induced Memory Impairment in Adults with Type 2 (link)

The Association Between High Blood Sugar & Cognitive Function

Source: J Gerontol A Biol Sci Med Sci. 2015 Apr; 70(4): 471–479 (link)

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5 Comments & Updates to “High Glycemic Brain Damage”

  1. JP Says:

    Updated 12/08/17:

    https://academic.oup.com/eurpub/advance-article-abstract/doi/10.1093/eurpub/ckx194/4621431?redirectedFrom=fulltext

    Eur J Public Health. 2017 Nov 13.

    Fasting plasma glucose in young adults free of diabetes is associated with cognitive function in midlife.

    Background: Evidence for an association of fasting plasma glucose (FPG) with cognitive function in adults free of diabetes is scarce and based on middle-aged and older adults. We examined the association of FPG, measured at age 30, and of change in FPG from age 30 to 43, with cognitive function at age 50.

    Methods: 505 nondiabetic participants of the population-based Jerusalem Lipid Research Clinic (LRC) cohort study had baseline FPG, 2-h post-oral challenge plasma glucose (OGTT) and insulin determined at ages 28-32, and FPG and OGTT again at ages 41-46. Subsequently at ages 48-52, global cognitive function and its five specific component domains were assessed with a NeuroTrax computerized test battery, using multiple linear regression and multivariable logistic models.

    Results: Hyperglycemia (FPG ≥ 5.6 mmol/l vs. <5.6 mmol/l) at baseline was associated with poorer global cognitive function in midlife (predominantly in the visual spatial and attention domains), independent of socio-demographic characteristics, life style variables, body mass index (BMI), and inflammatory and biochemical variables (standardized Beta = -0.121, P = 0.002, plinear trend(FPG continuous) =0.016). Similarly, increased odds for low-ranked (lowest fifth) global cognition was evident (ORper mmol/l FPG=2.31, 95% CI = 1.30-4.13, P = 0.005). Baseline OGTT, insulin resistance (HOMA-IR) and change in FPG and OGTT over 13 years were not associated with cognition.

    Conclusion: A higher FPG in young adults was associated with lower cognitive performance in midlife. Although we cannot dismiss the possibility of reverse causation, hyperglycemia at a young age may be a modifiable risk factor for low-ranked cognitive function in midlife.

    Be well!

    JP

  2. JP Says:

    Updated 12/08/17:

    https://www.frontiersin.org/articles/10.3389/fnagi.2017.00072/full

    Front Aging Neurosci. 2017 Mar 23;9:72.

    The Associations among Insulin Resistance, Hyperglycemia, Physical Performance, Diabetes Mellitus, and Cognitive Function in Relatively Healthy Older Adults with Subtle Cognitive Dysfunction.

    Insulin resistance (IR), diabetes mellitus (DM), sarcopenia, and cognitive dysfunction are thought to be mutually associated. We conducted a comprehensive assessment of the relationships among IR, gait speed, hyperglycemia, and DM by cross-sectionally analyzing the baseline data of an interventional study for cognitive preservation with physical exercise (the TOyota Preventional Intervention for Cognitive decline and Sarcopenia [TOPICS]). The participants (n = 444) were relatively healthy older individuals who had mild cognitive impairment without dementia, and 61 of the participants had DM. Slow gait speed and hyperglycemia were associated with cognitive dysfunction, mainly in the executive function domain, whereas IR was associated with memory impairment. The participants with DM had lower general cognition and executive function. Executive dysfunction in the DM participants seemed to be partly explained by hyperglycemia and/or slow gait speed. Our findings confirmed that IR, DM, sarcopenia, and cognitive dysfunction are mutually associated in complex ways. Understanding the mechanisms underlying these associations will lead to effective strategies to prevent and treat cognitive dysfunction in older individuals.

    Be well!

    JP

  3. JP Says:

    Updated 12/08/17:

    http://www.clinicalnutritionjournal.com/article/S0261-5614(17)30250-9/fulltext

    Clin Nutr. 2017 Jul 17. pii: S0261-5614(17)30250-9.

    Association between glycemic load and cognitive function in community-dwelling older adults: Results from the Brain in Motion study.

    BACKGROUND: Impaired glucose tolerance is a risk factor for non-age-related cognitive decline and is also associated with measures of physical activity (PA) and cardiorespiratory fitness (CRF). A low glycemic load (GL) diet can aid in the management of blood glucose levels, but little is known about its effect on cognition with poor glucoregulation.

    OBJECTIVE: We assessed the relation between GL and cognitive function by glucoregulation and possible mediatory effects by CRF and PA in older adults from the Brain in Motion Study.

    DESIGN: A cross-sectional analysis of 194 cognitively healthy adults aged ≥55 years (mean = 65.7, SD = 6.1) was conducted. GL was assessed using a quantitative food frequency questionnaire, and glucoregulation was characterized on the HOMA-IR index. Subjects also completed a cognitive assessment, CRF testing, a validated self-reported PA questionnaire, and a blood draw. Multiple linear regression models adjusted for significant covariates were used to evaluate the relation between GL and cognition, and mediation by CRF and PA was also assessed.

    RESULTS: GL was inversely associated with global cognition (β = -0.014; 95% CI -0.024, -0.004) and figural memory (β = -0.035; 95% CI -0.052, -0.018) in subjects with poor glucoregulation. Neither CRF nor PA mediated these relations. In subjects with good glucoregulation, no association was found between GL and cognitive function (p > 0.05).

    CONCLUSIONS: A low GL diet is associated with better cognitive function in older adults with poor glucoregulation. This study provides supportive evidence for the role of GL in maintaining better cognitive function during the aging process.

    Be well!

    JP

  4. JP Says:

    Updated 12/12/17:

    https://academic.oup.com/nutritionreviews/advance-article-abstract/doi/10.1093/nutrit/nux052/4713926?redirectedFrom=fulltext

    Nutr Rev. 2017 Dec 8.

    Flaxseed supplementation on glucose control and insulin sensitivity: a systematic review and meta-analysis of 25 randomized, placebo-controlled trials.

    Context: The results of human clinical trials investigating the effects of flaxseed on glucose control and insulin sensitivity are inconsistent.

    Objective: The present study aimed to systematically review and analyze randomized controlled trials assessing the effects of flaxseed consumption on glycemic control.

    Data Sources: PubMed, Medline via Ovid, SCOPUS, EMBASE, and ISI Web of Sciences databases were searched up to November 2016.

    Study Selection: Clinical trials in which flaxseed or its products were administered as an intervention were included.

    Data Extraction: The outcomes were fasting blood glucose, insulin concentration, insulin resistance (HOMA-IR), insulin sensitivity (QUIKI), and hemoglobin A1c (HbA1c).

    Results: A total of 25 randomized clinical trials (30 treatment arms) were included. Meta-analysis suggested a significant association between flaxseed supplementation and a reduction in blood glucose (weighted mean difference [WMD], -2.94 mg/dL; 95%CI,  -5.31 to - 0.56; P = 0.015), insulin levels (WMD,  -7.32 pmol/L; 95%CI, -11.66 to -2.97; P = 0.001), and HOMA-IR index (WMD, -0.49; 95%CI,: -0.78 to - 0.20; P = 0.001) and an increase in QUIKI index (WMD, 0.019; 95%CI, 0.008-0.031; P = 0.001). No significant effect on HbA1c (WMD, -0.045%; 95%CI, -0.16 to - 0.07; P = 0.468) was found. In subgroup analysis, a significant reduction in blood glucose, insulin, and HOMA-IR and a significant increase in QUIKI were found only in studies using whole flaxseed but not flaxseed oil and lignan extract. Furthermore, a significant reduction was observed in insulin levels and insulin sensitivity indexes only in the subset of trials lasting ≥12 weeks.

    Conclusions: Whole flaxseed, but not flaxseed oil and lignan extract, has significant effects on improving glycemic control. Further studies are needed to determine the benefits of flaxseed on glycemic parameters.

    Be well!

    JP

  5. JP Says:

    Updated 12/22/17:

    https://www.ncbi.nlm.nih.gov/pubmed/29263222

    Neurology. 2017 Dec 20.

    Nutrients and bioactives in green leafy vegetables and cognitive decline: Prospective study.

    OBJECTIVE: To increase understanding of the biological mechanisms underlying the association, we investigated the individual relations to cognitive decline of the primary nutrients and bioactives in green leafy vegetables, including vitamin K (phylloquinone), lutein, β-carotene, nitrate, folate, kaempferol, and α-tocopherol.

    METHODS: This was a prospective study of 960 participants of the Memory and Aging Project, ages 58-99 years, who completed a food frequency questionnaire and had ≥2 cognitive assessments over a mean 4.7 years.

    RESULTS: In a linear mixed model adjusted for age, sex, education, participation in cognitive activities, physical activities, smoking, and seafood and alcohol consumption, consumption of green leafy vegetables was associated with slower cognitive decline; the decline rate for those in the highest quintile of intake (median 1.3 servings/d) was slower by β = 0.05 standardized units (p = 0.0001) or the equivalent of being 11 years younger in age. Higher intakes of each of the nutrients and bioactives except β-carotene were individually associated with slower cognitive decline. In the adjusted models, the rates for the highest vs the lowest quintiles of intake were β = 0.02, p = 0.002 for phylloquinone; β = 0.04, p = 0.002 for lutein; β = 0.05, p < 0.001 for folate; β = 0.03, p = 0.02 for α-tocopherol; β = 0.04, p = 0.002 for nitrate; β = 0.04, p = 0.003 for kaempferol; and β = 0.02, p = 0.08 for β-carotene.

    CONCLUSIONS: Consumption of approximately 1 serving per day of green leafy vegetables and foods rich in phylloquinone, lutein, nitrate, folate, α-tocopherol, and kaempferol may help to slow cognitive decline with aging.

    Be well!

    JP

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