A 2011 study by Gu & Scarmeasfound participants whose dietary pattern included a higher intake of fruits, vegetables, fish, nuts, and legumes, as well as a lower intake of meats, high fat dairy, and sweets reduced their risk of developing Alzheimer’s disease (AD) and age-related dementia (ARD).  Similarly, a literature review by Demarin, Lisak, & Morovic (2011), found people following a Mediterranean diet enjoyed a reduced risk for a wide range of neurodegenerative diseases such as AD, Parkinson’s, and other cognitive impairments.  Solfrizzi et al. (2011), found that the MedDiet reduced both the risk of Alzheimer’s disease and the rate of progression from the beginning stages of dementia to moderate-to-severe dementia.

A substantial amount of well-documented, quantitative evidence has been collected from numerous studies detailing test score improvements.  Scarmeas et al. (2009), found participants who closely followed the Mediterranean diet had a 28% lower risk of developing cognitive impairment over a 4.5-year period than those who didn’t follow the diet.  Also, volunteers suffering from some form of cognitive impairment at the start of the study who followed the Mediterranean diet had a 48% lower risk of developing full-blown Alzheimer’s disease than those who didn’t follow a Mediterranean diet by the end of the study.

The Mediterranean diet also appeared to increased life expectancy for people already suffering from AD.  Scarmeas et al. (2009), found that AD patients who followed the MedDiet very closely for a period of 4.4 years were 76% less likely to die than those who followed it the least.  Even a loose adherence to the MedDiet increased life expectancy.  AD patients who followed the Mediterranean diet to only a moderate degree lived an average 1.3 years longer than those who adhered to the diet to the least degree.

Inflammation is a well-known cause of many chronic diseases; including cardiovascular diseases, type 2 diabetes, cancer and AD (Nield, 2016).  A growing number of epidemiological studies have found that following a MedDiet can reduce inflammation.  Close adherence to a MedDiet has been shown to cause a decrease in both white blood cell and platelet counts, two common measures of low-grade inflammation.

Martinez-Lapiscina et al. (2013), found that the MedDiet was significantly better at preserving brain function than a low-fat diet.  The researchers studied 522 male and female volunteers between the ages of 55 and 80 who were healthy, but were at a higher risk for AD and dementia because of risk factors such as high blood pressure, family history, or being overweight.

The participants were split into three groups.  The first group followed a MedDiet and consumed at least a half-liter of extra virgin olive oil each week.  The second group followed a MedDiet plus a daily serving of nuts. The third control group ate a modern low-fat diet.  All study subjects took extensive cognitive tests at baseline and again 6 1/2 years later.  The tests gauged higher cognitive functions such as language skills, time and place orientation, abstract thinking and memory.

95 participants had developed either AD or MCI by the end of the study. 30 of the participants who consumed a MedDiet plus olive oil developed AD or MCI, while 25 who had followed the MedDiet plus nuts developed dementia, and 40 participants who followed the low-fat diet had either MCI or AD.  The follow-up cognitive function test showed that, on average, those who followed either one of the MedDiets scored substantially higher than those following the low-fat diet.

Martinez-Lapiscina et al. (2009), double-checked their findings by following up with 285 people. Participants averaged 67 years old at the start. Once again, participants were split into three equivalent and random groups; a MedDiet plus olive oil group, a MedDiet plus nuts group, and a low-fat diet control group. Their diets were documented using a self-report food questionnaire.

Study subjects cognitive acuity was tested at baseline and four years later. Again, the researchers found that olive oil was especially good for cognition. The group that ingested additional olive oil was 66% less likely to develop cognitive impairment at the conclusion of the study as the low fat diet control group.

Because of the relatively small sample size, results from both studies were not definitive. However, Martinez-Lapiscina et al. said it was one of the first times improvements in cognitive function have been linked to adherence to a Mediterranean diet in a randomized trial.

A study for the American Academy of Neurology by Luciano et al. (2017) found that older adults who followed a traditional MedDiet retained more grey matter as they get older than those who didn’t follow a MedDiet.  The study measured changes in brain volumes of 562 mentally healthy participants for 6 years from a large group of Scottish people designated as the “Lothian Birth Cohort.”  The study subjects were all born in 1936 and had taken standardized health assessments throughout their lives, including a mental ability test when they were 11 years old.

Around the time they reached 70, participating Lothian Birth Cohort members filled out dietary frequency forms that informed researchers what kinds of foods they ate and which kinds of foods they avoided.  Luciano et al. (2017), used the dietary surveys to split the volunteers into two groups; those who followed a Mediterranean-style diet and those who did not.  Using magnetic resonance imaging (MRI) scans, researchers gave participants a baseline brain scan
at age 70, and then again three and six years later to measure any changes in brain volume.  Other key factors taken into consideration were body mass index, diabetes, high blood pressure, cardiovascular disease history, IQ and years of education.

The MRI scans found that the brains of participants who followed the Mediterranean diet shrank about half as much as those who didn’t.  Even individuals who only loosely followed the Mediterranean diet had significantly less brain shrinkage.  The study also found that participants with a wide range of IQs and educational backgrounds benefited from the diet.  This suggests that the Mediterranean diet did not just help more educated or intelligent individuals who, generally speaking, tend to have larger brain volumes.  Luciano et al. (2017), said the study’s lengthy seven-year duration helped establish scientific evidence that the brain-shrinkage rates were tied to dietary patterns, and weren’t just flukes or casual associations.

Another important question concerning dietary interventions is what time of life should you start and when is it too late to start?  Evidence from a couple of recent studies suggest when it comes to making better dietary choices the sooner, the better.  But just about anyone, regardless of age or physical condition, can benefit from better nutrition at any age.

In a large cohort study of more than 10,000 healthy women, Samieri et al. (2013), found that women who followed a healthy Mediterranean diet in their 50s and 60s were 40% more likely to be cognitively healthy and live disease-free past the age of 70.

Researchers recorded each participants diet and overall health in the mid 1980s, then checked back with them 15 years later.  They found that women who ate balanced, healthy diets were 34% more likely to age healthily than women who ate less-healthy diets.  Women following a Mediterranean diet fared even better, they were 46% more likely to live disease free well past the age of 70; avoiding chronic illnesses such as heart disease, diabetes, and Parkinson’s disease.  They also showed far less cognitive impairment compared to the less healthy control group.

Researchers reported that women who ate more plant-based diet were healthier than those who didn’t.  They said a plant-based Mediterranean diet rich in whole grains, legumes, fruit, and vegetables is filled with fiber that helped reduce oxidative stress, slow digestion and control blood sugar.

While sooner may be better, a randomized controlled Scandinavian trial found that it’s never too late to benefit from a dietary change.  Kivipelto et al. (2015), recruited a group of 1,260 people in Finland considered at risk of dementia who were between the ages of 60 and 77.  Half of the participants followed a standard diet while the other half ate a modified Mediterranean diet and took part in a low-impact exercise plan.

Participants in the Mediterranean diet intervention group ended up doing substantially better on standardized cognitive tests.  Participants in the intervention group scored 25% higher on a neuropsychological test compared to the control group.  The differences in memory improvement was even greater. The intervention group scored 83% higher in executive memory tests, and processing speed was 150% faster that the control group.  Best of all, researchers said those improvements became apparent within just two years.

Kivipelto et al. (2015), said while previous research showed causal links between cognitive decline and lifestyle factors, theirs was the first large randomized controlled trial to show that an intensive program aimed at addressing these risk factors might be able to prevent cognitive decline in elderly people.

Olive oil, a central component of the MedDiet, was found to improve brain health in a French study conducted by Berr et al., (2009). Researchers followed 6,947 people ages 65 and over living in 3 French cities for 5 years.  Study subjects were split into three groups; no olive oil use at all, moderate use for cooking, and intensive use for both cooking and dressing. 23% of study participants used no olive oil, 40% used it moderately, and 37% were intensive users.  Outcomes were adjusted for overall health, lifestyle behaviors, socio-economic factors and other dietary considerations.

Participants in the Berr et al. (2009), study were given a series of cognitive tests at baseline and then again 4 years later.  The tests measured visual memory, verbal fluency, and overall cognitive function.  The researchers found that intensive use of olive oil resulted in a 17% reduction in cognitive decline and a 15% reduction of verbal fluency decline.

Several additional confounding factors could have influenced the findings. Intensive olive oil users were three times more likely to eat fish at least twice a week and two times more likely to have three or more vegetable servings a day than participants who used no olive oil.  Berr et al. (2009), wrote that olive oil in-and-of itself could most likely help improve cognition later on in life.  But overall diet, especially fruit and vegetable intake, were critically important for long-term health benefits.

A significant drawback of Berr et al.’s (2009), research, besides being a cohort and not a controlled study, was that researchers defined the moderate use category as “cooking only.”  Many of the nutrients in olive oil are heat sensitive. The “cooking only” category could have ruined many nutritional components, including monounsaturated fats and other cell-protecting antioxidants.  Only the “intensive” category participants used olive oil in salad dressings and drizzled it over their vegetables, which would preserve the heat-sensitive nutrients.  The researchers recommended a follow-up study to adjust for this line of inquiry.

Olive oil is considered to be so healthy because olives contain a large number of medicinal phytonutrients.  A principal phytonutrient is oleuropein, with is an antioxidant proved to reduce blood pressure and inflammation.  Other olive oil phytonutrients include hydroxytyrosol, tyrosol, and verbascoside (Mercola, 2016).

Extra virgin olive oil is the healthiest method of producing the oil. Extra virgin has the most antioxidants because the olives are processed naturally and crushed with a mechanical press.  Lesser grades of olive oil use chemical solvents or hot temperatures to extract the oil, methods that degrade the oil’s polyphenol content.

In addition of olive oil, fruits and vegetables are primary sources of healthy antioxidants, which help prevent damage to the brain and body by stabilizing rogue molecules known as free radicals.  Free radicals can damage cells and other genetic materials (Moeller, 2002).  Two types of extremely toxic free radicals already mentioned are tau tangles and beta-amyloid plaques.

A 2002 study by Engelhart et al., followed the dietary habits of more than 5,000 women and men who were at least 55 years old for an average of 6 years to examine the long-term effect of antioxidants on cognitive function.  All study subjects were healthy at the beginning of the study with no signs of AD or ARD.  The researchers analyzed the participant’s diets for antioxidant consumption at baseline, then gave them medical examinations and cognitive assessments every year after that to look for signs of dementia throughout the duration of the study.  Six years later, 197 study subjects had developed AD or ARD.

Researchers found that smokers who regularly ate foods rich in antioxidants were 70% less likely to develop AD than smokers who did not have high antioxidant diets. Smokers seemed to gain the most benefit from vitamins C and E, as well as from beta-carotene.  Nonsmokers did not gain same level of benefits from antioxidants.  The researchers noted that smoking could dramatically increase the body’s production of free radicals.

A study by Morris (2009), found that food rich in vitamin E appeared to decrease rates of cognitive decline and help a significant number of study subjects reduce their risk for AD and ARD.  Researchers recruited 815 older adults ages 65 and older.  They used self-report food frequency questionnaires to determine how much vitamins C, E and beta-carotene participants consumed at baseline and for 4 years after that.  131 people developed AD during the four-year study period.

Morris noted that increased levels of vitamin E for participants in the highest percentile resulted in a 43% decreased risk for AD.  However, this decreased risk was only found in participants who didn’t have the APOE-4 allele, a protein associated with an increased risk for AD.

A potential drawback with both the Morris (2009), and Engelhart et al. (2002), studies was that participants with cognitive problems might not be able to accurately report their diet or supplement use.  Also, both researchers noted that anyone who was concerned they were suffering from memory loss might start eating more healthily or taking more vitamin and mineral supplements.

It’s also been noted that the closer you follow a traditional Mediterranean diet, the better your chances are of preventing AD.  A study from Columbia University Medical Center in New York City by Scarmeas et al. (2006), followed 2,258 older people for four years, focusing on how a close adherence to a traditional Mediterranean diet influenced the brain health of study subjects developing AD. It was one of the first studies focusing on the Mediterranean diet’s effect on AD and cognitive decline as a whole, and not just individual types of food.

To make sure they were healthy and lacked cognitive impairment, participants were given a baseline standard medical and neurological examinations.  The neurological exam consisted of short and long-term memory tests, orientation, abstract reasoning, language and comprehension.  Participants were split into three groups according to their Mediterranean diet adherence using two seven-day food records.  The results were adjusted for age, sex, ethnicity, and education, smoking, comorbidity index, and body mass index.

After four years, 262 participants developed AD or dementia.  Scarmeas et al. (2006), found that participants who closely followed a traditional Mediterranean diet were 40% less likely to develop Alzheimer’s than people who only loosely followed the MedDiet.  And, as a general rule, study subjects who developed dementia were older, less educated, and had lower body mass indexes.

The ratios between Mediterranean diet and developing AD remained constant, even after adjusting for potential confounders such as age, sex, ethnicity, education, and body mass index.  Scarmeas et al. (2006), said a high intake of fish, fruits, and vegetables rich in antioxidants, plus an emphasis on unsaturated fats combined to lower the risk for developing AD.  The biggest drawback of the study is that it didn’t stop to consider the possible additive and interactive effects of all the different types of nutritional components working together.

Results from several prospective studies cited here suggest that the Mediterranean diet can reduce the risk of developing AD and ARD.  However, the results are not all consistent, which could be caused by differences in populations of study participants.  The Health, Aging, and Body Composition study (Health ABC) was a longitudinal cohort study that (Atkinson et al., 2007). The Health ABC study began in 1997 and followed 2,326 older adults in Memphis, TN and Pittsburgh, PA for 10 years.  Researchers used food-frequency questionnaires to determine how closely participants followed the Mediterranean diet as regards race and gender.  38.2% of participants were African-American, 51.3% were females aged 70-79 at the beginning of the study.

Atkinson et al. (2007), say the study found that a closer adherence to the Mediterranean diet reduced the rate of cognitive decline among African-American seniors, but not white senior citizens.  Researchers said the differences may be explained by socioeconomic factors which can be associated with both diet and cognitive performance.  The highly complex relationship between socioeconomic factors and race may cause some residual confounding. The discrepancy in outcomes might also be influenced by cardiovascular disease.  Researchers cite the example that African-Americans are known to be more sensitive to sodium intake and prone to high blood pressure.

The research indicates that a Mediterranean diet can help reduce both oxidative stress and inflammation and is made up of several dietary components thought to improve overall brain health.  It can also improve vascular risk factors such as diabetes and hypertension.  Researchers found that African-American who followed the Mediterranean diet closely declined significantly less on follow-up cognitive tests than those who didn’t follow it as closely. The difference was 22 points per year after adjusting for external factors like age, sex, education, physical activity, depression, diabetes and socioeconomic status.  Participants in the highest adherence group also had 15% lower homocysteine levels (Atkinson et al., 2007).

Limitations of the study include not distinguishing between different types of food categories, frequencies of food intake.  Additional randomized controlled trials with more diverse populations are needed to help confirm the association between the Mediterranean diet and cognitive decline.  If race does play a significant factor, additional studies using multiethnic cohorts can help discover whether a cognitive benefit is due to genetic or environmental factors.  Atkinson et al. (2007), conclude by saying regardless of any potential confounding race effects, following a MedDiet is still recommended for its many health benefits.  It is also likely that a lower adherence to a Mediterranean diet could be a consequence and not a cause of AD or ARD.

Sources

The DASH diet was designed to lower sodium intake.  The average American’s diet contains some 3,400 mg of sodium a day.  There are two versions of the DASH diet.  The original diet allows up to 2,300 mg of sodium a day.  A revised diet reduces sodium for people with hypertension to only 1,500 mg a day (Heller, 2016).  Both DASH diets emphasize eating vegetables, fruits, and low-fat dairy.  DASH dieters can eat moderate amounts of whole grains, fish, poultry, and nuts.  Lean red meat, sweets, and fats are allowed, but only in small amounts.

To assess the cognitive benefits of the DASH diet Smith et al. (2010), recruited 124 participants with elevated blood pressure who were sedentary and had body mass indexes between 25 and 44.  Participants were randomly assigned to three groups for the four-month study; a DASH diet but no exercise group, a DASH diet plus exercise group, and a control group that didn’t exercise or follow the DASH diet.

The DASH diet only group were shown how to modify their diet but received no exercise encouragement or instructions.  The DASH diet plus exercise group was given the same dietary advice but also attended three 30-minute aerobic exercise programs per week in addition to a weekly half-hour group counseling session that focused on weight loss.  The control group did not amend their diet or exercise routines.

To assess physiological changes, researchers took high-resolution ultrasound images of the participant’s brains at baseline and again after the four month intervention to measure common carotid arteries.  Common carotid arteries are jugular arteries that supply oxygenated blood to the head and neck.  To measure any cognitive performance changes, study subjects were given several neurocognitive tests at baseline and again four months later to assess executive function, memory, and psychomotor speed.

Researchers found the DASH diet plus exercise group experienced significant improvements in neurocognitive function compared to the sedentary control group.  The DASH diet plus exercise group scored an impressive 6.1-year improvement on the four-month follow-up test that measured the time it took them to identify and differentiate colors and words from a list.  Conversely, the sedentary control group scored an 11.7-year poorer performance on the same test. Similar gains were found on the follow-up psychomotor speed test with both the DASH plus exercise and the DASH alone groups relative to the control group.  In addition, participants in both active treatment groups had lower blood pressure than the control group.

The biggest shortcoming of the Smith et al. study was it’s short four-month time frame. Researchers say they don’t know whether the benefits of the DASH diet plus exercise and DASH diet alone groups are temporary, or are things that can be maintained over time. The study does not reveal the underlying physiological mechanisms that improved cognitive function. Researchers also note that cognitive gains could be caused by a reduction in inflammation and other unknown neurochemical changes.

Both the DASH diet and the Mediterranean diet are very similar.  Both are based on heart-healthy eating habits that emphasize natural, unprocessed foods.  Both are rich in fruits and vegetables, whole grains, legumes and nuts.  Both diets encourage eating unsaturated fats, while saturated fats, sugar, and empty calories are strongly discouraged.  Both diets are also relatively flexible.  Finally, both promote long-term lifestyle changes rather than short-term fixes or dietary fads.

The main differences between the DASH diet and Mediterranean diet is that the DASH diet is more structured and emphasizes portion control and calorie restrictions, where as the Mediterranean diet doesn’t mention portion size or recommend specific amounts of any food group (Özkurt, 2015).  Both diets limit saturated fat intake, but the Mediterranean diet’s focus on olive oil means that it is more likely to be a high fat and calorie diet.  It’s also possible that the Mediterranean diet may be more heart-healthy due to the fact that it’s cholesterol-lowering properties.

Another important difference between the two diets is the DASH diet allows for two to four servings of dairy products each day.  Given the scarcity of dairy products in many parts of the Mediterranean region, many people following the Mediterranean diet can often go for days at a time without any dairy products.  And, while the DASH diet recommends daily lean red mean consumption, the Mediterranean diet mostly excludes red meat and recommends that some form of fish or seafood be eaten on a daily basis (Özkurt, 2015).

Given their many similarities, it’s not surprising several studies have conducted head-to-head comparisons of the DASH diet and Mediterranean diet.  Tangney et al. (2014), compared the two diets at how effective they were at slowing down cognitive decline in older adults.  826 older adults with an average age of 81.5 years were recruited for the prospective cohort study.

To help determine diet, participants filled out a self-report 144-item food frequency questionnaire at baseline.  They were also a cognitive assessment at baseline and at least two more over the four-year course of the study. Participants were assigned to three groups based on dietary scores monitoring how closely they adhered to either the DASH or Mediterranean diet.

Researchers then compared the DASH and Mediterranean groups relative rates of cognitive decline to a control group that followed a typical carbohydrate-rich diet.  The researchers found that both the DASH and Mediterranean dietary patterns resulted in slower rates of cognitive decline that were roughly the same.  Additionally, cognitive brain age testing scores for participants who followed the DASH diet the closest were at least 4.4 years younger than the group that followed it the least.  The study also found after the four-month intervention that learning and psychomotor function improved significantly for participants following the DASH dietary plan.  The researchers noted that findings from similar studies suggest that the cognitive benefits gained from the DASH diet may come quickly.

Researchers say they don’t know the underlying physiological reasons why the DASH and Mediterranean diet helped improved cognitive function, but they theorized that one main factor may be lower inflammation levels.  Reduced levels of inflammation have been found among people following both dietary patterns.  Inflammation is known to damage brain cells.  Also, the antioxidant protections provided by both the DASH diet and Mediterranean diet have been found to help protect against hypertension, obesity, diabetes, and cardiovascular disease.  Medical conditions that have all been linked to AD and cognitive decline.

Because the characteristics of both diets are so similar, Tangney et al. (2014), suggest the diets focus on natural, minimally processed foods and a reduced consumption of saturated fats may be more important than the specific diet type. Researchers said the findings point toward the need for more studies focusing on food-based approaches preventative and mitigating effects on cognitive decline. Researchers concluded by saying the stakes for finding out if diet can help prevent AD and vascular dementia have never been higher, considering the rapidly growing population of older adults at risk for the diseases.

Up next, a closer look at a brain-healthy diet that provides a significant cognitive boost even if you don’t follow all that closely.

Heller, M. (2016, April 4). What is the DASH diet? Retrieved from: http://dashdiet.org/ what_is_the_dash_diet.asp

Marcason (2015), says one of the MIND diets biggest advantages is that it’s easier to follow than the Mediterranean diet, which is challenging for many people because it requires the frequent consumption of fish along with several daily servings of fruit and vegetables.  The MIND diet is easier to follow because it recommends more accessible and affordable fruits, vegetables and low-fat dairy.

A common thread running through all three brain healthy diets is that they are all plant-based and low in saturated fats.  The MIND diet is broken down into 15 food groups which are made up of ten brain-healthy elements and five unhealthy elements.  The ten brain-healthy groups include: green leafy vegetables, other vegetables, nuts, berries, beans, whole grains, fish, poultry, olive oil and wine.  The five food groups to be avoided are red meats, butter and stick margarine, cheese, pastries and sweets, and fried or fast food.  The suggested daily servings for the MIND diet include three servings of whole grains, a salad and one other vegetable, plus a glass of wine. In addition, snacking most days on nuts and beans is suggested.  Eating poultry and berries at least twice a week and fish at least once a week is also recommended (Marcason, 2015).

Morris et al. (2015), conducted an extensive study that assessed the dietary habits of more than 900 older adults ages 58 to 98 for five years.  Diet type was determined by a self-reporting food frequency questionnaire filled out at baseline and every year after that.  Cognitive function was also evaluated at baseline and at the conclusion of the study by two standardized qualitative tests.  Researchers found that seniors who closely followed the MIND diet for five years cut their risk of developing AD by as much as 53%.

Researchers also compared the long-term effects of the Mediterranean diet, DASH diet and MIND diet.  During the 4-1/2 year period, 144 out of the 923 volunteers developed AD.  They found that all three diets provided significant protection against AD and dementia when followed closely.  The Mediterranean diet lowered AD and ARD risk by 54%, the MIND diet lowered it by 53%, and the DASH diet reduced the risk of developing dementia by 39%.

However, an important difference between the MIND diet and the other two diets was found in the areas of adherence and results.  Protective brain benefits were negligible when participants only loosely followed either the DASH or Mediterranean diet.  But, as indicated earlier, even a marginal compliance to the MIND diet lowered AD risk by as much as 35% (Morris et al., 2015).Another positive finding from the Morris et al. study (2015), was that the longer people followed the MIND diet, the greater the cognitive benefits.  The brain age of the top third tertile of those most closely following the MIND diet was an equivalent of 7.5 years younger than those in the bottom third at, the conclusion of the study.

Another positive finding from the Morris study was that the longer people followed the MIND diet, the greater the cognitive benefits.  The brain age of the top third tertile of those most closely following the MIND diet was an equivalent of 7.5 years younger than those in the bottom third at, the conclusion of the study.

Among the drawbacks of the Morris et al. (2015), studies were the research was observational, not randomized or controlled, which didn’t yield any hard scientific evidence.  Instead, the research only showed an association between the two. In order to establish a cause-and-effect relationship between the MIND diet and lowered risk of AD.  A randomized controlled study is needed to examine whether combining diet with other lifestyle interventions like exercise and medications can provide additional benefits.

Eat Your Veggies

It turns out your mother was right, you really should eat your vegetables.  A study funded by the National Institutes of Health (Morris et al., 2015 March 30), found eating dark leafy green vegetables can take years of wear and tear off both your body and your brain.  Researchers followed the diets and measured the cognitive function of 954 senior citizens from Chicago’s Rush University Memory and Aging Project for five years.  On average, participants were 81 years old at the start of the study. More than 70% were women.  To determine nutritional patterns, study subjects filled out a self-report 144-item food and drink survey about the types and quantities of food they ate on a daily basis once a year for the duration of the study.  Participants were given a battery of 19 quantitative tests every year to measure cognitive function.  Results of the tests were adjusted for sex, age, smoking, and education.

Researchers distilled the individual nutrients in the diets down to the ones they thought to be responsible for improved brain performance.  They eventually concluded that vitamin K was a principal agent leading to slower cognitive decline.  Researchers found that study participants who ate more spinach, kale, collards and mustard greens had significantly lower rates of cognitive decline than those who didn’t.  They concluded that beta-carotene, lutein, and other minerals in leafy green vegetables also helped improve or maintain cognitive function.  At the end of the five-year study, people who ate one or two servings of leafy green vegetables per day scored the equivalent of 11 years younger on cognitive tests than those who didn’t eat any vegetables.

The study concluded by saying more research is needed to help determine exactly which nutrients in leafy green vegetables benefit the brain. The researchers warned that the study focused exclusively on food sources of vitamin K. They noted that it is extremely difficult, if not impossible, to separate vitamin K from the other nutrients found in the fresh vegetables.

Sources

The brain needs lots of energy to work properly. While accounting for only about 2% of adult body weight, the brain accounts for about 20% of the body’s energy use and 16% of the body’s total oxygen supply (Harris, Jolivet & Attwell, 2012).  Although the brain prefers to run on glucose blood sugar, it can also burn ketones in a pinch when glucose is unavailable.  Ketones are small fuel molecules produced from fat by the liver.  The body starts producing ketones only after running out of carbohydrates, which is a metabolic survival adaptation response to preserve strength and increase chances of survival, usually as a result of starvation or prolonged fasting.

Once the body starts producing ketones, it’s in a state called ketosis and begins to run almost exclusively on fat (Gasior, Rogawski & Hartman, 2006).  The Ketogenic Diet (KD) mimics the effects of starvation to get the body to produce ketones. The KD eliminates sweets, starchy carbs, and grains. It also limits fruit consumption and allows for only moderate amounts of protein. It is similar to the Atkins, South Beach and other low carb, high fat diets. The difference between the KD and low fat, high fiber diets is the KD restricts proteins, which are converted into blood sugar if too many are in the bloodstream (Eenfeldt, 2017).

There are many ancillary benefits to a KD.  Insulin levels drop, and since blood sugar levels are lowered, a KD is a very effective way to treat type 2 diabetes.  Fat burning is dramatically increased, which is great for weight loss.  The KD is also used to treat epilepsy.  Epilepsy patients were first put on a KD more than 90 years ago after doctors observed that it reduced or eliminated seizures.  Many high endurance athletes also favor a KD because it dramatically increase physical stamina. Although the body’s supply of carbohydrates run out after a few hours, fat stores fueling ketone production can provide a steady source of energy for days at a time (Henderson, 2006).

A KD can also help cognitive function.  Ketosis sends a steady stream of ketones to the brain, avoiding the big swings found with carbohydrates and blood sugar based diet.  A KD allows people suffering from AD and dementia to increase mitochondrial efficiency and give the brain an alternative fuel source (Eenfeldt, 2017).  This is critical for AD and dementia patients because one of the first things that happens to people suffering from AD is a significant decline in the brain’s ability to metabolize glucose.  Studies comparing AD patients to people with healthy brains found a 17% to 24% decline in the cerebral rate of glucose metabolism, which is thought to be a cause of amyloid plaque buildup and brain cell atrophy that so often characterizes AD (Henderson, 2006).

Most of the oxygen in the brain is used to oxidize glucose into carbon dioxide and water, which can cause extensive oxidative damage.  The brain is protected by three cell barriers, called the blood brain barriers.  Glucose can’t get through these semi-permeable barriers on it’s own, it needs to bond to specific transport proteins to cross over.  The levels of these brain glucose transporters are significantly decreased in patients with AD.  Several studies have found that even when some areas of the brain can no longer use glucose in the early stages of AD, there is evidence to suggest they are still able to burn ketones (Gasior, 2006).

Cunnane et al. (2016), conducted a systematic review that found that the brain is still able to burn ketones even in someone with AD or dementia who is suffering from deteriorating glucose uptake.  What’s more, researchers found that AD and ARD patients showed appreciable improvements in cognitive function when their ketone levels were raised, suggesting that the troubled areas of the brain were not dead, but simply dormant and waiting for a usable supply of energy.

The researchers concluded that AD and ARD can be made worse by chronic brain fuel starvation caused by brain glucose deficit.  The researchers went on to say that treating AD and dementia with ketogenic interventions is safe, ethical, and scientifically well-founded.  They suggest that oral ketogenic supplements are the fastest and most effective way to provide ketones to people suffering from mild cognitive impairment and early AD (Cunnane et al., 2016).

Reger et al. (2004), organized a crossover study to see if injecting a single shot of medium chain triglycerides would jumpstart ketosis and improve cognitive function in older adults with mild cognitive impairment and AD.  Medium chain triglycerides are healthy types of fat most commonly found in coconut and palm oils.  They go straight to the liver, where they are converted into ketones.  Because they have shorter chain length than more complex fatty acids, medium chain triglycerides are quickly broken down and absorbed by the body.

The researchers injected 20 people with mild-to-moderate AD a 40-gram dose of soluble ketone bodies called beta-hydroxybutyrates.  The shot increased ketone levels by a factor of 10 after just two hours.  Researchers hypothesized that elevated ketone levels would boost brain energy and temporarily improve cognitive performance without the need to wait for a long-term ketogenic diet to take effect.  They tested the volunteers at baseline and 90-minutes after injection with a variety of quantitative cognitive tests (Reger et al., 2004).

All 20 subjects scored higher 90-minutes after being injected with the medium chain triglycerides.  The medium chain triglyceride serum led to better performances across-the-board, particularly on a memory-intensive paragraph recall test.  Not surprisingly, volunteers with higher ketone levels made the biggest gains.  Reger et al. (2004), said such a dramatic increase after such a short time with no other external variables suggests the improvements in test scores were caused by increased neuronal metabolisms spurred by elevated ketone levels.

Reger’s et al. (2004), preliminary results were followed up four years later in a larger and longer-term analysis of the effects of daily oral ingestion of medium-chain triglycerides on cognitive function in mild to moderate AD patients.  Henderson et al. (2009), conducted a double-blind, placebo-controlled, multi-center trial on 152 volunteers at 23 different clinical sites across the United States. Volunteers were randomly split into an intervention group and a control group. Both groups stayed on a normal diet and continued to take any prescribed AD medications.  Ketosis was induced by giving study subjects a daily measure of 20 grams of an oral ketogenic compound called AC-1202 for 90 days.

Subjects blood levels were tested at baseline, and then again at 45 and 90 days.  Results from the 45 and 90 days tests showed that the daily dose of medium chain triglycerides triggered significant increases in serum ketone levels.  Two hours after ingesting the medium chain triglycerides, mean ketone levels rose to 0.36mM on the 45th day, and 0.39mM on the 90th day.  Quantitative cognitive test scores improved for the entire intervention group.  After 45 days, study subjects taking ketogenic compounds made a noteworthy 1.9-point mean gain over the control groups on standardized tests.

However, findings from both studies suggest that the cognitive benefits of induced ketosis may largely depend upon genetics. In the earlier Reger et al. (2004) study, medium chain triglycerides only improved cognitive function in participants who lacked the APOE4 gene, a known genetic risk factor for AD. In the later Henderson et al. (2006) study, cognitive improvements were much more pronounced for those lacking the APOE4 gene. Volunteers without the APOE4 gene showed an impressive 5.3 point gain from baseline ADAS-cog scores on the 90th day assessment. Both studies found that higher ketone levels correlated with improved test scores, suggesting ketosis may be helpful for AD patients, particularly if they lack the APOE4 gene (Henderson et al., 2006).

It should be noted, however, that the levels of ketosis achieved in the Reger et al. (2004), and Henderson et al. (2006), studies were substantially lower than levels used in previous, long-term infusion studies. The research suggests that the body responds quickly to medium chain triglycerides and can easily build levels of ketosis that may provide potentially life-changing benefits for AD patients.

These promising early findings on the effects of medically administered ketogenic compounds offered hope that a KD might be able to impart real, long-term brain benefits.  A 2012 study by Krikorian et al., tested whether a ketogenic diet would improve memory in older adults without administering or injecting medical supplements.  Researchers recruited 23 older adults with mild cognitive impairments.  The study subjects were randomized.  Half were put on a KD for 6 weeks, with just 5 to 10 percent of calories coming from carbohydrates.  The control group ate a typical high-carbohydrate diet, with at least 50 percent of their calories coming from carbohydrates.

After six weeks, Krikorian et al. (2012), found participants following a KD showed significant improvements in verbal memory compared to the control group.  The verbal memory assessments tested the participants recall of words and other abstractions.  Researchers found the higher the ketone levels, the better the verbal memory.  Researchers said the findings indicated that ketosis can improve memory function in older adults, even those with an increased genetic risk for AD.

However, the researchers also pointed out that the cognitive gains may have been partially due to a reduction of excess insulin in the blood which, as mentioned earlier, is known to hamper cognitive function.  The researchers said that other mechanisms associated with ketosis such as reduced inflammation and oxidative stress say have also led to improved cognitive function (Krikorian et al., 2012).

Besides improvements in cognitive function, Krikorian et al. (2012), said study subjects following the KD also lost weight and had reductions in blood glucose and insulin levels. Taken as a whole, these results indicate that ketosis, in the short term at least, offers many advantages for both the brain and body.

A major drawback of all three ketogenic studies were their limited time frames. Researchers questioned whether the benefits of a low-carbohydrate diet remained after someone returned to a normal diet. If a KD has cognitive and physical benefits that last beyond the intervention period, it might be a strategy people can uses intermittently to help ease concerns over adverse effects of long-term carb restrictions.

Although some studies have analyzed the short-term effects of a ketogenic diet, very few have looked into the long-term effects. One concern about following the ketogenic diet is a gradual loss of bone mineral content. Due to time and money constraints, most controlled nutritional studies typically last anywhere from 12 weeks to a year. Clearly, this is too short a time to gauge long-term effects on the human body.

Bertoli et al. (2014), set out to examine the long-term effects of a KD on body composition and bone health. The researchers studied the bone health of three adult women with glucose transporter 1 deficiency syndrome (Glut1) who’d been following a KD from more than five years. Glut1 is a rare genetic disorder where patients lack a key protein needed to transport glucose across the blood-brain barrier. This condition leads to debilitating and potentially life threatening complications that include severe epileptic seizures, developmental delays, and cognitive decline. Doctors have prescribed a KD to counteract Glut1 for more than 80 years because it helps control epileptic seizures.

The three Bertoli et al. (2014), subjects underwent standard blood testing and an abdominal ultrasound, as well as body composition and bone mineral status measurements at baseline, and then again on an annual basis for the next five years. They were also given standardized neurologic examinations and cognitive tests along the way. All three subjects experienced a rapid and complete disappearance of paroxsmal dyskinesias, an epileptic condition characterized by sudden and often severe episodes of involuntary and uncontrollable movements, as soon as ketosis took effect.

Researchers found that long-term adherence did not produce any appreciable changes in weight or body fat. In fact, muscle strength increased in all three patients. There was also no evidence of adverse effects on bone health after five years. Cognitive function did not change appreciably for any of the study subjects (Bertoli et al., 2014).

These findings stand in direct contrast to previous studies focusing on small children suffering from Glut1 deficiencies (Bertoli et al., 2014). The Researchers found that children with intractable epilepsy following a prolonged KD resulted in a progressive loss of bone mineral content. Researchers theorized the bone loss is associated with poor bone heath, most likely as a by-product of a chronic acidic environment. The discrepancy in the findings might be explained by the fact the the the Glut1 patients were adults and had normal bone mineralization at baseline.

The main drawback of the Bertoli et al. (2014), study is it’s limited scope of just three participants. Subsequent studies need to broaden their focuses to larger populations to confirm and expand the findings.

While it’s generally accepted that a KD helps protect the brain from neurodegeneration, little is known about how ketones actually work. Van de Auwera et al. (2005), tested a KD on mouse models to investigate the specific processes. 16 mice were put on two different diets for 43 days. The control group was kept on a standard high carbohydrate/low fat diet, the intervention group was put on a high fat/low carbohydrate KD. Both groups had unlimited access to food.

The results surprised the researchers. Van de Auwera et al. (2005), thought that the high fat/low carbohydrate diet would cause an increase of plaques in the brain, but post-mortem autopsies revealed that mice following the KD experienced a 25% decrease in beta amyloid plaques and tau tangles compared to the high-carbohydrate, low-fat diet control group. The researchers said the findings indicate that anyone designing a dietary strategy to reduce harmful plaques in the brain should first consider how dietary components influence biochemistry and metabolic outcomes. Particular attention should be given to the levels of fats, carbohydrates, total calories, and presence of ketone bodies. Obvious drawbacks to this study include the short time frame and the reality that the mouse models may not accurately represent human molecular mechanisms.

Carb Cycling

One of the biggest drawbacks for active and athletic people following a KD is a lack of carbohydrate powered energy. It is possible to take a more moderated approach to KD called “carb cycling”. Carb cycling schedules a couple of carb-loading binge days every week to allow the body replenish it’s carbohydrate stores. The goal of carb cycling is not for the dieter to be in a ketogenic state all the time but to be able to easily slip in and out of ketosis (Haque, 2015).

A weeklong carb cycling strategy typically involves five or six days of a strict ketogenic diet, followed by one or two carbohydrate binge days. Carb loading days allows physicallyactive dieters to replenish depleted glycogen stores in their muscles. Glycogen helps them maintain a sufficient level of strength for their workouts (Haque, 2015).

Carb cycling is effective for athletes because once glycogen reserves are depleted, new carbs go straight to the muscles and liver, instead of the body’s fat stores. An added benefit of carb cycling is that it gives dieters a break from the relative drudgery of following a KD, which can be great for psychological well-being as well as long-term willpower.

To start carb cycling, dieters follow a strict 10 to 14 day “induction phase” where they follow a low carb diet to induce ketosis. Once they achieve ketosis, they slowly progress onto the cyclical diet where they follow the same carb cycling pattern every week. Because the glycogen goes straight to the muscles and liver on a carb cycling diet, the amount of calories consumed can be significantly greater than usual. A typical carb cycling ketosis day is limited to 50 grams or less of carbs. Binge days can include upwards of 450-600 grams of carbs (Haque, 2015).

Haque (2015), concludes that the biggest drawback of carb cycling is that it can be complex and hard to follow. Carb cycling requires the dieters to keep close track of the number of carbohydrate grams they eat. The re-feed process can also be a delicate balancing act because it can lead to significant fat gain if more carbs are consumed than are needed to replenish glycogen stores.
Risks and Drawbacks of a KD

Because switching to a KD is a significant lifestyle change, there are several short-term side-effects. As stated earlier, the brain prefers to run on glucose, so it will burn the very last stores before switching over to ketones. The worst physical reactions from a KD resemble the flu and are most evident during the first week of the diet. The first symptom is fatigue and dizziness. Headaches, nausea, and muscle cramps are other common side-effects. These symptoms are caused by low levels of minerals such as salt, magnesium, and potassium. This so-called “induction flu” eases after the body switches over to ketosis (Smith, 2015).

Other common complications include weight loss, constipation, and increased cholesterol and lipid levels. Women might also experience disruptions to the menstrual cycle. Another side- effect is the need to urinate more frequently. This is because the body is burning up glucose deposits stored in the liver and muscles. Breaking down this stored glucose down requires lots of water. The kidneys also start discharging excess sodium as insulin levels drop. These effects are usually temporary, and ease as the body adjusts to ketosis (Smith, 2015).

Smith (2015), suggests several things that can help manage the side-effects of a KD. Multivitamins, calcium and vitamin D supplements help ease the symptoms. Ingesting more salt and eating foods rich in potassium such as dairy, leafy green vegetables and avocados is also recommended.