The average American consumes somewhere between two to three pounds of sugar each week. Over the last twenty years, our national sugar consumption exploded from 26 pounds to 135 pounds of sugar—per person—annually. Compare that to sugar consumption in the late 1800s, when the average consumption was five pounds per person-per year. A time, incidentally, when heart disease and cancer were virtually unknown.
While your brain requires a pretty constant supply of the blood sugar product glucose in order to function properly, constantly eating refined sugars and slurping down sodas does not provide the best route for sugar intake. On the contrary, researchers at the Salk Institute in California found that high glucose levels resulting from quick, easy sugar intake slowly but surely damage cells everywhere in the body, especially those in the brain.
Unfortunately, having too little glucose and having too much glucose are both problematic. When your blood sugar levels drop, your hypothalamus sends out a distress signal that leads to the release of adrenaline to your liver, ordering it to turn excess fat into glucose.
When you consume too much sugar, your pancreas secretes insulin to nudge that extra sugar into your cells, and too much insulin can deplete your normal glucose levels, depress your immune system, and lead to kidney disease.
Plus, excess insulin also promotes fat storage, which sets up a vicious cycle. Either extreme can leave you feeling woozy, nervous, fatigued, and shaky.
Two additional reasons why excess refined sugar is detrimental to your brain:
- A research group at the University of Wisconsin found that the brain may react to excess refined sugars found in food as if they were a virus or bacteria. The resulting immune response may cause cognitive deficits such as those associated with Alzheimer’s disease.
- High blood sugar coupled with performing a mentally challenging task is associated with high levels of cortisol—a stress hormone known to impair memory.
In other words, that second piece of cake at the company birthday party might stress out you, your body, and your brain . . . and affect your afternoon work efficiency!
Your Brain on Sugar
It’s pretty clear—excessive glucose in the form of refined sugar can be very detrimental to your brain, ultimately affecting your attention span, your short-term memory, and your mood stability. Excessive refined sugar can:
- Block membranes and thereby slow down neural communication.
- Increase free radical inflammatory stress on your brain. Free radicals can rupture cells.
- Interfere with synaptic communication.
- Cause neurons to misfire and send erroneous messages that take time and energy to sort out.
- Increase delta, alpha, and theta brain waves, which make it harder to think clearly.
- Can eventually damage your neurons.
Is There Such a Thing as Healthy Sugar?
Not really . . . a simple sugar is a simple sugar. However, those occurring in real food, such as fructose in fruit and lactose in milk, also provide other nutrients so are slightly more healthy than any other sugar. And even though health food stores love to promote honey, molasses, maple syrup, or agave as natural sweeteners, they are still simple sugars, with the same fattening calories and little nutritive value as refined white sugar. They do, however, tend to be a tad sweeter, so maybe you’ll be happier with a smaller amount, but don’t kid yourself about them being healthier. Sugar is sugar, and you need to limit how much you consume on a daily basis.
Go Light on the Honey, Honey
Although honey is a natural sweetener, 96 percent of honey consists of the simple sugars fructose, glucose, and sucrose. Honey also has the highest calorie content of all sugars with 65 calories per tablespoon, compared to the 48 calories per tablespoon found in table sugar. The increased calories are bound to cause increased blood serum fatty acids, as well as weight gain, on top of the risk of more cavities.
Why Soda Crashes and Burns Your System
Your brain uses 65 percent of your body’s glucose, but too much or too little glucose can have a detrimental effect on brain function. One can of soda contains 10 teaspoons of table sugar, all of which floods into a blood stream that typically contains a total of 4 teaspoons of blood sugar. The rush alerts your pancreas to release a lot of insulin. Some sugar is quickly ushered into the cells, including brain cells, and the rest goes into storage or into fat cells. An hour later, your blood sugar may fall dramatically, creating low blood sugar, and these rapid swings produce symptoms of impaired memory and clouded thinking.
Actually we have studies dating back to the 1970’s and even earlier showing that the entire cycle of sugar and carbohydrate addiction is induced by a deficiency of serotonin. Serotonin is known to be the “happy” neurotransmitter and it can only be made in the brain from protein. Because sugar does nothing to replenish depleted serotonin, it’s hard to break the addiction cycle.
The natural food supplements L-tryptophan and 5HTP provide the brain with more of the raw material it needs to make serotonin. The same studies mentioned above also showed that when people take these supplements in appropriate doses their cravings abate and their consumption of carbohydrates and overall calories decrease. (J Pharm Pharmacol 1975 Jan; 27 (1): 31-7; Brain Res Bull 1986 Nov; 17 (5): 681-9; Pharmacol Biochem Behav 1986 Oct; 25 (4): 711-6; J Neurol Transm 1989; 76 (2): 109-17).
Armed with this knowledge, physician Marty Hinz, MD, has built a large and successful practice focused entirely on treating weight problems with these types of supplements. Dr. Hinz has also stated repeatedly that in his experience – spanning more than a decade and thousands of patients – these amino acid (protein) supplements work better for appetite control than any medication, including the ill-fated phen-fen combination. For more on Dr. Hinz and his work visit www.neuroreplete.com.
To my friends who love to drink alcohol be it San Miguel beer or red wine, do eat protein rich foods like soft boiled eggs when drinking.
To my BFF with pancreas health issues, eat soft boiled eggs.
Acetylcholine/Choline Deficiency in Chronic Illness – The Hunt for the Missing Egg.
Those who lack choline are prone to mental illness, heart disease, fatty liver and/or hemorrhagic kidney necrosis and chronic illness as choline is oxidized to betaine which acts as an important methyl donor and osmolyte. With fatty liver, a person can be prone to diabetes and other chronic illness. Eggs are rich in choline. Choline is also found in a wide range of plant foods in small amounts. Eating a well-balanced vegan diet with plenty of whole foods should ensure you are getting enough choline. Soymilk, tofu, quinoa, and broccoli are particularly rich sources.
We hear a lot about vitamins and minerals such as B12, folate, magnesium, vitamin C, and so on, but there seems very little talk these days on the importance of dietary lecithin and choline. Are you consuming an adequate amount of acetylcholine, or other phospholipids? The odds are that you are not.
A little bit about choline
The human body produces choline by methylation of phosphatidylethanolamine (from dietary sources such as lecithin and others) to form phosphatidylcholine in the liver by the PEMT enzyme. Phosphatidylcholine may also be consumed in the diet or by supplementation. Choline is oxidized to betaine which acts as an important methyl donor and osmolyte.
For those wanting to see how this relates to the methylation cycle, below is a nice graphic (courtesy of Wikipedia).
It is well known that magnesium deficiency is widespread (57% of the population does not meet the U.S. RDA according to the USDA), but the numbers for choline deficiency are even more shocking.
According the National Health and Nutrition Examination Survey (NHANES) in 2003-2004, only about 10% of the population have an adequate intake of choline. This means about 90% of the population consumes a diet deficient in choline. Furthermore, those without an adequate intake of choline may not have symptoms.
Along with folate and B12 deficiency, inadequate consumption of choline can lead to high homocysteine and all the risks associated with hyperhomocysteinaemia, such as cardiovascular disease, neuropsychiatric illness (Alzheimer’s disease, schizophrenia) and osteoporosis. Inadequate choline intake can also lead to fatty liver or non-alcoholic fatty liver disease (NAFLD).
The most common symptoms of choline deficiency are fatty liver and/or hemorrhagic kidney necrosis. Consuming choline rich foods usually relieve these deficiency symptoms. Diagnosing fatty liver isn’t as simple as running ALT and AST since nearly 80% of people with fatty liver have normal levels of these enzymes according to a population study published in the journal Hepatology. In fact, in an experiment, 10 women were fed a diet low in choline. Nine developed fatty liver and only one had elevated liver enzymes.
Estrogen and Choline Deficiency
Given the connection between low lipids and choline deficiency, it would be tempting to think that as long as someone has enough cholesterol and TG that they will be protected from choline deficiency. Unfortunately this is not the case. Having adequate lipids does indeed help support healthy choline levels, but it does not guarantee a person will avoid choline deficiency. The truth is that choline deficiency can come from more than one source. Both sex hormone levels and genetic SNPs may lead to a choline deficiency by influencing the PEMT enzyme – the enzyme responsible for synthesis of choline inside the body. Recent research now confirms how hormones and genetic polymorphisms play a major role in choline deficiency.
The body can make choline only one way; that is by methylating a molecule of phosphatidylethanolamine (PE) into a molecule of phosphatidylcholine (PC). The body’s only method for accomplishing this is via the enzyme PEMT (phosphatidylethanolamine N-methyltransferase) which is found in the liver, brain, muscle, fat and other tissues.1,2 As with other well-known methylation enzymes like MTHFR and COMT, the PEMT enzyme can have genetic SNPs that slow it down. When this enzyme slows down the body cannot make choline in high amounts and choline deficiency is more likely. But there is more to the story of PEMT than just polymorphisms. In addition to being slowed by SNPs, PEMT is also dependent upon the hormone estrogen for activation. 1, 3 What this means is that the PEMT enzyme, the body’s only method of synthesizing choline, has not one but two Achilles heals. The PEMT pathway and how it relates to phosphatidylcholine production is shown in Figure 1.3 below.
Figure 1.3 – PEMT is shown as the rate-limiting reaction in the production of phosphatidylcholine inside the human body. Due to genetic and hormonal variances, most people have a PEMT enzyme working too slow and are susceptible to choline deficiency when there is not enough choline in the diet. ACoA – Acetyl-CoA; TG – Triglycerides; PE – phosphatidylethanolamine; PC – phosphatidylecholine; PEMT – phosphatidylethanolamine N-methyltransferase.
As mentioned above, the sex hormone estrogen is intimately linked with the production of choline. Women have a biological advantage here as the premenopausal female body has much higher levels of estrogen than does the male body. When a woman becomes pregnant this advantage is taken to an extreme, as pregnancy increases estrogen levels over 30 times normal.4 A successful pregnancy requires high amounts of nutrients delivered to the growing baby, esp. choline. Since the mother’s body is building a human being from scratch, there is an added burden on her biology to provide enough nutrition to her growing baby. Viewed from this perspective, the high estrogen levels during pregnancy can be seen to act like a biochemical insurance policy. Since the PEMT enzyme requires estrogen to function, pregnancy allows a woman to make extra choline for her developing child. Furthermore, the nervous system is the first system to form in utero and is a tissue that requires high levels of choline for proper development.5, 6 Choline plays such an important role in cell membranes, myelin sheaths, and nervous system tissue that the high estrogen levels during pregnancy help make sure the growing brain and nervous system is nourished. It is a genius system that assures the health and survival of the child.
Even though Nature has conferred an advantage to females by providing them with higher estrogen levels, esp. during pregnancy, this alone cannot protect against a lack of choline in the diet. All the estrogen in the world will not save a woman from choline deficiency if the gene responsible for producing choline is slowed down by a polymorphism. Genetic research has shown that the gene responsible for synthesizing choline, the PEMT gene, is susceptible to common polymorphisms which alter its function by slowing it down. In a recent study looking at a population in North Carolina, men and women of various ages were placed on a choline-deficient diet. They were followed closely for up to 42 days on a low choline diet consisting of less than 50mg choline per day. Throughout the study, the participants’ liver function was continuously assessed for any sign of fatty liver and damage. After eating a choline deficient diet for just six weeks, 63% of participants developed liver dysfunction and choline blood levels dropped 30% in every single participant, including premenopausal females.7 During this six week trial of low dietary choline the odds of developing liver dysfunction were 77% for men, 80% for postmenopausal women and just 44% for premenopausal women.7 Based on what has been discussed so far about estrogen and choline, it makes sense that men and postmenopausal women would be more susceptible to developing fatty liver since they don’t have high estrogen levels. And based on the fact that estrogen levels drive choline production, premenopausal women should have been protected from fatty liver since they make higher amounts of choline – but that was not the case.
With dietary choline restricted to just 50 mg/day, approximately half of the premenopausal group also suffered liver dysfunction, suggesting that a choline deficient diet can even harm women with higher estrogen levels. In addition, blood tests revealed that premenopausal female experienced a 30% loss of choline on a low choline diet right along with everyone else. Despite the fact that higher estrogen levels allow fertile women to make more choline, many were not able to make enough to avoid problems. A PEMT gene polymorphism is the only mechanism that can explain how women with high estrogen levels are still susceptible to choline deficiency when placed on a low choline diet.
Just like many individuals in the population, some of the premenopausal women inherited one or two copies of the PEMT gene which slows down the production of choline. This study showed that fatty liver occurred in 80% of the premenopausal women with two copies of PEMT and in 43% with only one copy of PEMT.8 What this means is that a premenopausal woman with two copies of the slowed PEMT gene has exactly the same risk of fatty liver as a postmenopausal woman. It is as if inheriting two copies of the PEMT gene effectively shuts off all estrogen-related choline production in the body. If a woman only has a single copy of the slowed PEMT gene, she will still have a roughly 50% chance of liver dysfunction on a low choline diet. Thus a single copy of the gene is only slightly better than two copies, as at least some estrogen-related choline production is preserved.
If having a PEMT gene can put one at risk for choline-related diseases like fatty liver, then it is important to know how common these genes are in population. We know that 74% of all women in the study had a SNP in the PEMT that made their PEMT enzyme unresponsive to estrogen.9 This means that only 26% of women can make enough choline on a low choline diet; and that ability depends on whether the woman is still fertile or has entered menopause. In this way genetics can take away the biological advantage that high estrogen levels usually offer to premenopausal females. Women with these PEMT genes will be at risk for choline deficiency and liver damage just like all men and post-menopausal women – two groups who don’t have enough estrogen to make choline regardless of their genes. Due to all the interference from the PEMT gene, dietary choline levels must be optimized for the vast majority of our population.
Summary of PEMT and Choline Deficiency:
- In humans, choline is only made by the PEMT enzyme
- Estrogen is required for the PEMT enzyme to activate and function normally
- Men and postmenopausal women have an elevated risk of choline deficiency due to low estrogen levels.
- The PEMT enzyme is commonly slowed down by polymorphisms, making it unresponsive to estrogen levels
- 74% of women have at least one copy of a slowed PEMT
- Homozygous carriers of PEMT have much higher risk of choline deficiency
- Men, postmenopausal women, and premenopausal women with PEMT SNPs need to increase choline intake in the diet to offset elevated risk of liver dysfunction
The take away here is that studies have recently shown that because of common genetic polymorphisms, choline deficiency is a widespread problem. Normally the hormone estrogen allows the body to make choline from scratch. However, genetic variation in the PEMT enzyme, estrogen levels and gender differences prevent most people from making adequate choline. Realistically then the only group in our population who is protected from choline deficiency are premenopausal females without a single copy of the slowed PEMT gene. Every single male, every single postmenopausal woman, and 74% of premenopausal woman all require daily intake of approx. 500 mg of choline to prevent fatty liver, organ damage, and the associated health problems.7 If the body is already depleted, then levels that simply prevent deficiency won’t be enough to replete the body. In these cases, higher daily doses of at least 1 gram or more are needed to replenish the tissues. Choline it seems must be absorbed from the diet in just about everyone except for the few young women who have a normal PEMT gene and can synthesize choline regardless of dietary intake.
BEST TO WORST WAYS HOW TO COOK EGGS FOR MAXIMUM NUTRITION: 1. SOFT BOILED. We’ll start out with the best way how to cook eggs for nutrition: soft boiled. This is when you boil anegg, but it is still a little runny and the yolk is definitely not hard. It might take a little more work than other methods, but soft boiled …
Oct 9, 2005 – I know that uncooked egg yolks are a source of choline (180-215mg?) and phosphatidylcholine. As I understand it, cooking the yolk kind of ‘denatures’ the choline and makes it unavailable. … Whole raw eggs are my source of choline and protien (and other stuff too).
There is a lot of speculation out there as to whether cooking an egg decreases the amounts of choline it contains. Most of what I see online says that it does. However, I have yet to find any scientific evidence that is the case. In fact, the USDA has a choline fact sheet, which has cooked eggs having slightly …
Oct 14, 2013 – A soft boiled egg contains useable lysine. Boil the egg for another minute to hard state, the lysine is not useable. Lysine is needed for the body to make use of the next 5 most important essential aminoes so that other aminoes can be made by the body. Lysine is denatured at about 110 degrees. As the heat …
Mar 5, 2015 – If you choose not to eat your eggs raw, poached or soft–boiled would be the next best option. This leaves the yolk still runny and the … Eggs also contain choline, selenium, biotin, B vitamins, phosphorus, and more, making them are one of the healthiest foods you can eat. And, contrary to popular belief, …
The ideal sources of choline are animal foods like egg yolks and liver, which contain the most concentrated amounts of this nutrient and can be easily incorporated into the diet to meet … Veggies from this group, including cauliflower, cabbage, bok choy and broccoli, boast around 65 mg of cholineper cup cooked.
Mar 28, 2013 – Hard-boiled eggs are commonly used for dying Easter eggs, but a soft–boiled egg can make a yummy breakfast or snack. How does … One large egg has about 75 calories, many essential nutrients, lots of high-quality protein, various vitamins, multiple minerals, choline, folate and riboflavin. Eggs can help …
Jun 7, 2014 – Eggs are a phenomenal source of protein, fat, and other nutrients, including choline and the antioxidants lutein and zeaxanthin. … While less “well done” eggs are still preferable (such as poached, soft-boiled, or over easy with very runny yolks), a hard-boiled egg makes a fine snack or source of protein for …
Feb 21, 2015 – This nutrient loss occurs regardless of whether the egg is removed from the shell (for example, during poaching) or left inside the shell during cooking (for example, during soft or hard boiling). If you compare the nutrient value of one large raw egg to one large hard-boiled egg in the latest version of the U.S. …
Eat Your Eggs! Choline and the Link With Fatty Liver. eggs “Stay away from eggs if you want to be healthy. They have all that fat and cholesterol!” If you’re like most people, you began hearing that information in the 70s, 80s or 90s (depending upon your age). …. I eate boiled eggs but not the yolk because I don’t like them.
Common Food Nutrient Tied to Risky Blood Clotting
By Amy Norton
Latest Heart News
MONDAY, April 24, 2017 (HealthDay News) — A nutrient in meat and eggs may conspire with gut bacteria to make the blood more prone to clotting, a small study suggests.
The nutrient is called choline. Researchers found that when they gave 18 healthy volunteers choline supplements, it boosted their production of a chemical called TMAO.
That, in turn, increased their blood cells’ tendency to clot. But the researchers also found that aspirin might reduce that risk.
TMAO is short for trimethylamine N-oxide. It’s produced when gut bacteria digest choline and certain other substances.
These findings, he said, give the first direct evidence that choline revs up TMAO production in the human gut, which then makes platelets (a type of blood cell) more prone to sticking together.
Choline is found in a range of foods, but it’s most concentrated in animal products such as egg yolks, beef and chicken.
Hazen said he and his colleagues at the Cleveland Clinic wanted to isolate the effects of choline on people’s levels of TMAO and their platelet function. So they studied supplements.
The researchers had 18 healthy adults –10 meat-eaters and eight vegetarians/vegans — take choline supplements for two months.
The supplements provided around 450 milligrams of choline daily — roughly the amount in two or three eggs, Hazen said.
One month in, the study found, the supplements had raised participants’ TMAO levels 10-fold, on average. And tests of their blood samples showed that their platelets had become more prone to clotting.
“This study gives us one of the mechanisms by which TMAO may contribute to cardiovascular disease,” said Dr. J. David Spence.
Spence, who was not involved in the study, directs the Stroke Prevention & Atherosclerosis Research Centre at Western University in London, Ontario, Canada.
For the healthy people in this study, Spence said, the TMAO rise from choline might not be worrisome. But, he added, it might be a concern for people at increased risk of heart disease or stroke.
Spence suggested those individuals limit egg yolks, beef and other foods high in choline.
Hazen had similar advice. “You don’t have to become a vegetarian,” he said. “But you could try eating more plant-based foods, and more vegetarian meals.”
He also pointed to the Mediterranean diet — rich in olive oil, vegetables and fish. In an earlier study, Hazen said, his team found that a compound in olive oil seems to inhibit TMAO formation.
The new study uncovered yet another compound that may counter TMAO: low-dose aspirin.
In a separate experiment, the researchers had some participants take 85 milligrams of aspirin (a baby aspirin) a day, in addition to choline supplements. That, it turned out, lessened the rise in TMAO and the change in platelet activity.
Doctors already prescribe low-dose aspirin to certain people at risk of heart disease and stroke.
It’s possible, Hazen said, that aspirin’s effects on TMAO are one reason it helps ward off cardiovascular trouble.
The current study is small and preliminary. But it’s the latest to suggest that the gut “microbiome” plays a key role in cardiovascular disease, Spence said.
The “microbiome” refers to the trillions of bacteria that dwell in the gut. Spence said researchers are just beginning to understand how gut bacteria and their byproducts affect the cardiovascular system.
But one hope, he said, is to figure out what balance of gut bacteria supports cardiovascular health — and possibly use probiotic (“good” bacteria) supplements to help treat people at high risk of heart disease or stroke.
Spence said his own lab is working on just that.
There are, of course, many factors in heart disease risk — from age to high blood pressure to diabetes to smoking, Hazen pointed out.
“We’re saying a portion of the risk is related to the gut microbiome,” he said.
Hazen and a colleague report potential royalty payments from several companies related to “cardiovascular diagnostics and therapeutics.” One company, Cleveland HeartLab, recently launched a test for measuring TMAO levels.
The findings appear in the April 25 online issue of Circulation.
Choline is an essential nutrient necessary for a wide range of functions from cellular maintenance to creating neurotransmitters. A deficiency in choline often appears as an increase in liver enzymes, and can lead to liver disease, heart disease, and even neurological disorders.
Health benefits of adequate choline include a reduced risk of dementia, cardiovascular disease, and cancer.2 Some studies have shown an increased risk of colon cancer with choline supplements, but natural food sources like those listed below are safe and healthy.
A daily value (DV) has not been established for choline, however, the adequate intake (AI) for adult men is 550mg a day for men and 425mg/day for women. High choline foods include liver, eggs, cauliflower, mushrooms, dark leafy greens, shellfish, asparagus, brussels sprouts, bok choy, and fish.
#1: Liver (Beef)
|Choline in 100g||Per Slice (81g)|
|418.2mg (76% AI)||338mg (62% AI)|
Other Liver Products High in Choline (%AI per 100g): Veal (73%), Chicken Liver (59%), and Chicken Liver Pate (42%).
|Choline in 100g||1 cup, chopped (136g)||1 large (50g)|
|293.8mg (53% AI)||399.6mg (72% AI)||146.9mg (27% AI)|
Most of the choline in eggs is contained in the yolk. Fish roe (eggs) are also a good source of choline providing 9% AI per tablespoon, and 17% AI per ounce
#3: Cauliflower (Raw)
|Choline in 100g||1 cup chopped (1/2″ pieces) (107g)||1 head medium (5-6″ dia.) (588g)|
|44.3mg (8% AI)||47.4mg (9% AI)||260.5mg (47% AI)|
Broccoli provides 5% AI per cup cooked
#4: Mushrooms (Cooked Shiitake)
|Choline in 100g||1 cup sliced (97g)||1 piece whole (19g)|
|59.4mg (11% AI)||57.6mg (10% AI)||11.3mg (2% AI)|
Other mushrooms high in choline (%AI per cup sliced): Oyster (8%), Portabella (7%), Enoki (6%), Maitake (6%), White Button (4%), and Brown Italian (Crimini) (3%)
#5: Dark Leafy Greens (Beet Greens, Cooked)
|Choline in 100g||1 cup (1″ pieces) (144g)|
|42.5mg (8% AI)||61.2mg (12% AI)|
Other dark leafy greens high in choline (%AI per cup cooked): Collards (14%), Swiss Chard (9%), and Spinach (6%). Click to see complete nutrition facts.
#6: Shellfish (Oysters)
|Choline in 100g||3 oz (85g)||6 medium (59g)|
|101mg (18% AI)||85.9mg (15% AI)||59.6mg (11% AI)|
Other Shellfish and Crustaceans High in Choline (%AI per 3oz (85g) serving): Shrimp (21%), Scallops (17%), Crayfish (13%), Crab (13%), and Lobster (13%)#7:
|Choline in 100g||1/2 cup (90g)||4 spears (1/2″ base) (60g)|
|26.1mg (5% AI)||23.5mg (5% AI)||15.7mg (3% AI)|
#8: Brussels Sprouts (Cooked)
|Choline in 100g||1/2 cup (78g)||1 sprout (21g)|
|40.6mg (7% AI)||31.7mg (6% AI)||8.5mg (2% AI)|
Cooked Cabbage provides 6% AI per cup cooked
#9: Cooked Bok Choy (Chinese Cabbage) (Pak-Choi)
|Choline in 100g||1 cup, shredded (170g)|
|12.1mg (2% AI)||20.6mg (3% AI)|
#10: Fish (Cod)
|Choline in 100g||3 oz (85g)||1 fillet (90g)|
|79.7mg (14% AI)||67.8mg (12% AI)||71mg (13% AI)|
Other fish high in Choline (%AI per 3oz (85g) serving): Salmon (18%), Pollock (14%), Flounder (Sole) (12%), Haddock (12%), Perch (12%)
There is accumulating evidence showing that lifestyle factors like diet may influence the onset and progression of Alzheimer’s disease (AD). Our previous studies suggest that a multi-nutrient diet, Fortasyn, containing nutritional precursors and cofactors for membrane synthesis, viz. docosahexaenoic acid, eicosapentaenoic acid, uridine-mono-phosphate, choline, phospholipids, folic acid, vitamins B6, B12, C, E, and selenium, has an ameliorating effect on cognitive deficits in an AD mouse model. In the present study we analyzed learning strategies and memory of 11-month-old AβPPswe/PS1dE9 (AβPP/PS1) mice in the Morris water maze (MWM) task performed after nine months of dietary intervention with a control diet or a Fortasyn diet to characterize diet-induced changes in cognitive performance. The Fortasyn diet had no significant effect on MWM task acquisition.
To assess hippocampus-dependent learning, the strategies that the mice used to find the hidden platform in the MWM were analyzed using the swim path data. During the fourth day of the MWM, AβPP/PS1 mice on control diet more often used the non-spatial random search strategy, while on the Fortasyn diet, the transgenic animals exhibited more chaining strategy than their wild-type littermates. During the probe trial, AβPP/PS1 mice displayed no clear preference for the target quadrant. Notably, in both transgenic and nontransgenic mice on Fortasyn diet, the latency to reach the former platform position was decreased compared to mice on the control diet. In conclusion, this specific nutrient combination showed a tendency to improve searching behavior in AβPP/PS1 mice by increasing the use of a more efficient search strategy and improving their swim efficiency by decreasing the latency to reach the former platform position.
Researchers have devised several lipid-based diets aimed at slowing down progression and relieving symptoms of Alzheimer’s disease.
Alzheimer´s disease (AD) is the most common disease underlying memory problems and dementia in the elderly. One of the invariable pathologies in AD is degeneration of cholinergic synapses in brain cortex and hippocampus. Despite enormous effort to find out an efficient treatment, current pharmacological interventions are limited to a few drugs that alleviate symptoms but do not slow down the underlying disease processes. These drugs include inhibitors of cholinesterases, enzymes that degrade the neurotransmitter acetylcholine, or memantine, a modulator of glutamate neurotransmission.
It is generally accepted that lifestyle and particularly dietary habits influence mental health, and prevalence and progression of AD. Numerous epidemiological studies have revealed profitable effects of dietary intake of especially fish oil on cognitive decline during aging and dementia.
Within the EU-funded project LipiDiDiet (FP7-211696), therapeutic and preventive impact of nutritional lipids on neuronal and cognitive performance in aging, Alzheimer´s disease and vascular dementia, researchers devised several lipid-based diets aimed at slowing down progression and relieving symptoms of AD. Short-term (3 weeks) feeding of young adult APPswe/PS1dE9 mice (transgenic mouse model of AD) with experimental diets containing fish oil or stigmasterol reversed the decrease in responsiveness of hippocampal muscarinic receptors to acetylcholine compared to their non-transgenic littermates. Only fish oil based diet enriched with nutrients supporting neuroprotection (Fortasyn diet) increased in addition the density of muscarinic receptors and cholinergic synapses in the hippocampus.
These findings yield important proof-of-principle evidence that regular intake of specific dietary components may help to prevent some of the key early functional changes that take place in the Alzheimer brain. These findings support viability of the dietary approach in AD.
Source: Faizan ul Haq – Bentham Science Publishers
Image Source: Image is in the public domain
Original Research: Abstract for “Lipid-Based Diets Improve Muscarinic Neurotransmission in the Hippocampus of Transgenic APPswe/PS1dE9 Mice” by Helena Janickova, Vladimir Rudajev, Eva Dolejsi, Hennariikka Koivisto, Jan Jakubik, Heikki Tanila, Esam E. El-Fakahany and Vladimir Dolezal in Current Alzheimer Research. Published online February 2016 doi:10.2174/1567205012666151027130350
Lipid-Based Diets Improve Muscarinic Neurotransmission in the Hippocampus of Transgenic APPswe/PS1dE9 Mice
Transgenic APPswe/PS1dE9 mice modeling Alzheimer’s disease demonstrate ongoing accumulation of β-amyloid fragments resulting in formation of amyloid plaques that starts at the age of 4-5 months. Buildup of β-amyloid fragments is accompanied by impairment of muscarinic transmission that becomes detectable at this age, well before the appearance of cognitive deficits that manifest around the age of 12 months. We have recently demonstrated that long-term feeding of trangenic mice with specific isocaloric fish oil-based diets improves specific behavioral parameters. Now we report on the influence of short-term feeding (3 weeks) of three isocaloric diets supplemented with Fortasyn (containing fish oil and ingredients supporting membrane renewal), the plant sterol stigmasterol together with fish oil, and stigmasterol alone on markers of cholinergic neurotransmission in the hippocampus of 5-month-old transgenic mice and their wild-type littermates. Transgenic mice fed normal diet demostrated increase in ChAT activity and attenuation of carbachol-stimulated GTP-γ35S binding compared to wild-type mice. None of the tested diets compared to control diet influenced the activities of ChAT, AChE, BuChE, muscarinic receptor density or carbachol-stimulated GTP-γ35S binding in wild-type mice. In contrast, all experimental diets increased the potency of carbachol in stimulating GTP-γ35S binding in trangenic mice to the level found in wild-type animals. Only the Fortasyn diet increased markers of cholinergic synapses in transgenic mice. Our data demonstrate that even short-term feeding of transgenic mice with chow containing specific lipid-based dietary supplements can influence markers of cholinergic synapses and rectify impaired muscarinic signal transduction that develops in transgenic mice.
“Lipid-Based Diets Improve Muscarinic Neurotransmission in the Hippocampus of Transgenic APPswe/PS1dE9 Mice” by Helena Janickova, Vladimir Rudajev, Eva Dolejsi, Hennariikka Koivisto, Jan Jakubik, Heikki Tanila, Esam E. El-Fakahany and Vladimir Dolezal in Current Alzheimer Research. Published online February 2016 doi:10.2174/1567205012666151027130350