I am going nowhere folks. Deal with it.
Not leaving : I am going nowhere folks... - Restless Legs Syn...
Not leaving
Of course you're not leaving. There's work to be done. Please read this and tell me what you think. It's long, it's boring, I LOVE it. How are you doing by the way? Did you read about that one woman on here who got some relief by switching out anti-d's? And another by switching heart medications? I'm telling you Mike, the RLS world is on the edge of a precipice. A few more pieces of good intel and these forums are going by way of horse and buggy. See below:
Interestingly, obesity is also associated with reduced number of receptors for dopamine, a neurotransmitter associated with pleasure or reward circuits in the brain. In 2001, Gene Jack Wang and Nora Volkow of the U.S. Department of Energy’s Brookhaven National Laboratory used Positron Emission Tomography (PET) brain scans to look at dopamine receptors in the brains of obese and normal individuals:
Obese individuals, the scientists found, had fewer dopamine receptors than normal-weight subjects. And within this obese group, the number of dopamine receptors decreased as the subjects’ body mass index, an indicator of obesity, increased. That is, the more obese the individual, the lower the number of receptors.
A 2008 study of women and adolescent girls in New Zealand showed that this receptor deficit is at least partly genetic. The overweight females had the Taq1A1 gene that is associated with fewer dopamine receptors. This receptor deficit in the obese led them to overeat to achieve the level of pleasure or satiety that normal individuals reached with less food. This reduced level of dopamine receptors tends to make life a bit less pleasant for the obese when they are hungry and without food. Ingestion of food, particularly carbohydrates, temporarily raises the level of dopamine, eliminating the “pleasure deficit” and rewarding eating behavior. Excessive eating or bingeing raises the dopamine levels even higher than normal, which can lead to a further downregulation of dopamine receptors, only worsening the craving problem. This effect is not only influenced by genes, but by diet; a 2010 study of rats fed a supermarket “junk food” diet showed raid desensitization of dopamine receptors a significant increase in appetite, and an unwillingness to return to eating “healthy” food.
The connection between obesity and the number and sensitivity of dopamine receptors is perhaps not so surprising, given how highly rewarding food can be for the obese; for many of the overweight, food becomes an addiction. It is still quite striking that this translates to such a significant decline in the number of dopamine receptors, while the baseline level of dopamine actually increases. Here, as with insulin and leptin, we have yet another example of reduced receptor levels being associated with obesity. By analogy with insulin resistance and leptin resistance, we might say that the strong appetite of the obese is a direct result of “dopamine resistance”.
2. Addiction. What is particularly interesting is that these low levels of dopamine receptors are also characteristic of drug addicts and alcoholics. Nora Volkow, one of the directors of the Brookhaven study, subsequently became director of NIDA, the National Institute of Drug Abuse. part of NIH, but her research on addiction actually predates the study she did on brain activity in the obese. She used PET brain scans to study dopamine receptors levels in alcoholics, cocaine addicts, and addicted smokers. And, as you might guess, the same pattern of reduced levels of dopamine receptors was observed in addicts vs. non-addicted controls. This is illustrated in the PET scan to the right, which shows dopamine binding activity for addicts (top row) vs. non-addicts (bottom row). Regions of greatest dopamine receptor activity are indicated with a color scale starting from red (most active), descending through yellow and green to blue and purple (least active).
The mechanism downregulation of dopamine receptors by cocaine has been elucidated:
Cocaine binds tightly at the dopamine transporter forming a complex that blocks the transporter’s function. The dopamine transporter can no longer perform its reuptake function, and thus dopamine accumulates in the synaptic cleft. This results in an enhanced and prolonged postsynaptic effect of dopaminergic signaling at dopamine receptors on the receiving neuron. Prolonged exposure to cocaine, as occurs with habitual use, leads to homeostatic dysregulation of normal (i.e. without cocaine) dopaminergic signaling via down-regulation of dopamine receptors and enhanced signal transduction. The decreased dopaminergic signaling after chronic cocaine use may contribute to depressive mood disorders and sensitize this important brain reward circuit to the reinforcing effects of cocaine (e.g. enhanced dopaminergic signalling only when cocaine is self-administered). This sensitization contributes to the intractable nature of addiction and relapse.
3. Depression. A reduced number or sensitivity of neurotransmitter receptors has also been linked to mood disorders such as major depression. Depression has been associated with shortages of at least two neurotransmitters: dopamine (which is associated with drive, motivation and pleasure), and serotinin (which is associated with a sense of well-being and pleasure). While dopamine receptors are located largely in the brain, a little known fact is that only about 20% of serotonin receptors are in the brain, most of the other 80% are in the gut, blood platelets, and other organs. That might help explain why serotonin is also associated with food and satiety. Different types or depression are often associated with a different imbalance of neurotransmitters, so despite the prevalence of SSRIs, which are intended to restore serotonin levels, some forms of depression respond better to antidepressants which boost dopamine levels.
While antidepressants work for many people, a surprising number — some estimates put it at 50% or higher — are unresponsive. Furthermore, long term use of SSRI’s can have the effect of downregulating serotonin (5-HT2A) receptors with adverse results:
Another adaptive process provoked by SSRIs is the downregulation of postsynaptic serotonin 5-HT2A receptors. After the use of an SSRI, since there is more serotonin available, the response is to decrease the number of postsynaptic receptors over time and in the long run, this modifies the serotonin/receptor ratio. This downregulation of 5-HT2A occurs when the antidepressant effects of SSRIs become apparent. Also, deceased suicidal and otherwise depressed patients have had more [presynaptic] 5-HT2A receptors than normal patients. These considerations suggest that 5-HT2A overactivity is involved in the pathogenesis of depression
The last sentence in the above quote again points to the fact that a deficiency of post-synaptic serotonin receptors, in combination with an excess of serotonin from diet, antidepressants, or elsewhere, may play a role in both the genesis and worsening of depression. The same phenomenon of receptor downregulation together with excess neurotransmitter has been noted with other antidepressants, such as MAO inhibitors and buproprion, that stimulate the production or prolong the lifetime of dopamine in the synapse. This can lead to tolerance and withdrawal effects.
In short, in all these cases — obesity, addiction, and depression — receptors are becoming less sensitive to a signaling compound as a reaction to excessive levels of that compound. So too much insulin and leptin lead to insulin and leptin resistance, too much dopamine to a downregulation of dopamine receptors.
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HOW TO UPREGULATE YOUR RECEPTORS. So if directly changing the amount of signaling compounds is frequently frustrated by receptor downregulation, is there anything you can do to upregulate the receptors? Fortunately, the answer is yes. There are a number of measures that have proven particularly effective for deliberately increasing the number and sensitivity of key classes of receptors:
Step 1: Strenuous exercise. Regular, intense exercise can upregulate your insulin receptors. In Dr. Bernstein’s Diabetes Solution, Richard Bernstein explains the role of exercise in actually reversing insulin resistance by growing new muscle tissue, and by increasing the density of glucose transporter receptors in muscle and other tissues. While his advice is directed primarily towards diabetics, it applies more broadly to anyone with some degree of insulin resistance That includes most of us. According to Dr. Bernstein:
The higher your ratio of abdominal fat to muscle mass, the more insulin-resistant you’re likely to be. As you increase your muscle mass, your insulin needs will be reduced…Long-term, regular strenuous exercise also reduces insulin resistance independently of its effect upon muscle mass…In my experience, it takes about two weeks of daily strenuous exercise to bring about a steady, increased level of insulin sensitivity…via increased production of glucose transporters in muscle cells. (DBDS, p. 170-1).
Furthermore, the exercise must be strenuous and “anaerobic” – not aerobic. There are two reasons for this:
First, the blood sugar drop during and after continuous anaerobic exercise will be much greater than after a similar period of aerobic exercise. Second, to accomplish efficient transport of glucose into muscle cells, as muscle strength and bulk develop, glucose transporters in these cells will greatly increase in number. Glucose transporters also become more numerous in tissues other than muscle, including the liver. (DBDS, p. 180)
Glucose transporter (GLUT4) receptors are upregulated by intense exercise. A study reported in the New England Journal of Medicine showed that this upregulation begins to happen within hours, but significant and sustained improvement requires repeated exercise sessions over several weeks. When insulin levels are kept low, the glucose transporters migrate from a location inside the cell to protrude beyond the cell surface, becoming more available to bind glucose and shepherd it into the interior of the cell. With time, the cells can actally express or “grow” additional receptors, increasing the overall rate of glucose transport. This increased response rate is synonymous with “insulin sensitivity”.
The benefits of anerobic exercise extend not only to upgregulation of insulin receptors, but also to maintaining high levels of dopamine “reward” receptors. A study of exercised rates by McRae et al at University of Texas showed that regular exercise has a protective effect on D2 dopamine receptors, while keeping levels of dopamine (DA) and dopamine metabolite (DOPAC) low. Unexercised rats saw both a decrease in D2 receptor density and an increase in circulating dopamine.
Step 2: Calorie restriction and intermittent fasting. Another brain scan study at Brookhaven National Laboratory showed that restricted eating led to higher numbers of dopamine receptors in obese rats:
The scientists found that genetically obese rats had lower levels of dopamine D2 receptors than lean rats. They also demonstrated that restricting food intake can significantly increase the number of D2 receptors, partially attenuating a normal decline associated with aging.
This research corroborates brain-imaging studies conducted at Brookhaven that found decreased levels of dopamine D2 receptors in obese people compared with normal-weight people,” said Brookhaven neuroscientist Panayotis (Peter) Thanos, lead author of the current study, which will be published online in the journal Synapse on Thursday, October 25, 2007.
One of the essential points to understand here is that if calorie restriction and intermittent fasting are effective, it is not for the reason that most people think explains this (that you are creating a calorie deficit). Rather, intense exercise and fasting work because they resensitize and grow your insulin and dopamine receptors in a way that allows you to get enough energy and pleasure from eating less food. This means that not only are the receptors upregulated, but you also get the energy and pleasure when you need it. So restricting calories is not good enough. You must eat foods that maximize insulin senstivity (e.g. containing adequate essential fatty acids, protein, magnesium, etc.) and foods which give you enough pleasure so as to satisfy your “pleasure budget”, but not so much as to downregulate your dopamine receptors. My experience is that intermittent fasting, using a varied diet, is the best way to do this. One reason that pure “starvation diets” like that used in the Minnesota Starvation Experiment may have failed is that the diet failed to supply adequate nutrients that to support receptor function for cellular energy and pleasure. (The 1560 calorie/day regimen consisted only of potatoes, rutabagas, turnips, bread and macaroni — so go figure!)
A particularly effective protocol for improving insulin sensitivity and upregulating glucose transporter receptors is called “fasted workouts”: a combination of intense exercise and intermittent fasting, in which eating is postponed until after one works out. One of the foremost practioners of this approach is Martin Berkhan, who I’ve referenced on the Fitness page of this blog, and whose Leangains blog I’ve listed under the Diet links. Martin summarizes the research by DeBock et al. and Cluberton et al. that documents the physiological beneifts of fasted workouts, including enhanced insulin sensitivity based upon a six-week study with four 60-90 minute workouts per week. The study controlled for dietary intake, and compared results of those who fasted (F) with the control group (C) that ate prior to working out. Among other variables, the study compared changes in the levels of the GLUT4 transporter, a type of insulin receptor in the muscles, between the F and C groups:
Glucose transporter type 4 is a protein responsible for insulin-regulated glucose transport into the muscle cell. It increased by a whopping 28% in F but only 2-3% in C (not mentioned in the paper but this is my estimate based on the graphs). This partly explains why F saw superior results in regards to glucose tolerance and insulin sensitivity. Since GLUT4 is triggered by AMPK, which is increased when glucose availability is low, i.e. during fasted training, one would assume the GLUT4 increase could then be explained by an increase in AMPK. This was found to be true: AMPK increased by 25% in F, which correlated closely with the increase in GLUT4 content.
Step 3: Deconditioning and extinction. Pleasure reward circuits do not change overnight. But the good news is that there is plenty of evidence that these reward circuits can be extinguished by classical conditioning techniques. I’ve discussed these deconditioning techniques in depth on the Psychology and Diet pages of this blog, and I’d recommend looking there for details. Extinction involves merely refraining from the undesired behavior (eating, addictive drugs) and allowing the cravings to happen without reinforcing them. It may surprise you how quickly your reward circuits recover, and it is very likely that this involves upregulation of dopamine receptors, so that the brain is more easily “satisifed” without the previously craved behavior. Deconditioning is more active than extinction; it requires actively exposing yourself to cues which normally set off the addictive response. This may sound extremely difficult, but is attested to by extensive research, as well as the personal experience of several people who have posted here on the Forum, including myself. One of the more successful appliations of active deconditioning is the Sinclair Method, which has been used successfully to extinguish alcoholism while training the former alcoholic to drink moderately. The key is the use of a dopamine blocker, naltrexone, to block the reward circuits during exposure.
Any type of extinction should benefit from simultaneous reinforcement of healthy alternative sources of pleasure, while engaging in exercise and intermittent fasting to rebuild the density and sensitivity of receptors. Unless you increase your level of dopamine receptors, you’ll always be vulnerable to the temptation of any pleasure that can “fill your pleasure deficit”.
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THE RECEPTOR CONTROL THEORY. Based upon a synthesis of extensive evidence, I’m putting forward in this post an alternative to the classic set point theory of Gordon Kennedy: the receptor control theory. This is a general hypothesis of biological regulation which applies to more than just weight control; it applies to any homeostatic variable that is controlled by cellular receptors — even, for example, pleasure and motivation. Whereas the classic set point theory of body weight posits a fixed genetic set point for each individual,
the receptor control theory postulates that our set points for regulating weight, energy, or pleasure are variable; they are directly related to the number, sensitivity and location of cellular receptors in our bodies, and can be modified by changing the number and sensitivity of these receptors.
For example, the set point for your body fat is controlled by insulin and leptin sensitivity, which is determined by the number and functional sensitivity of insulin and leptin receptors throughout your body. As the number and sensitivity of insulin and leptin receptors decreases, body weight set point goes up. But unlike the set point theory, body fat set point can also go down by increasing the number and sensitivity of these receptors — for example by the use of strenuous exercise, intermittent fasting, and extinction.
If you don’t change the number and sensitivity of your receptors, your set point will not change. Under these circumstances, the receptor control theory agrees with the classic fixed set point theory. However, the receptor control theory provides a way to change your set point by upregulating your receptors.
The pleasure budget. The receptor control theory goes beyond weight management to explain more generally the regulation of pleasure in your life. If you have ample dopamine receptors, then a wide variety of stimuli– including food, social interactions, work, and other interests– should provide you with sufficient pleasure to make life not just bearable, but interesting. However, if you end up with an undersupply of dopamine receptors — whether it be from birth, addictions or unremitting stress — then your baseline pleasure “set point” will be low and you’ll be vulnerable to depression, low self-esteem and other aspects of unhappiness. Addictive escapes may provide temporary (but unsustainable) bursts of dopamine, serotonin, and other feel-good neurotransmitters, but at the cost of further downregulating dopamine receptors and feeling worse later on.
Oops, wait, left out the beginning part about RLS...hold on.
Hmmm, well, here's a two second to read article. Which led to the above much longer and much more detailed information which does not directly address RLS but talks about how to "upregulate your d2 receptors."
medica-tradefair.com/cipp/m...
It is estimated that five to ten percent of adults in the United States have RLS. The disorder often has a substantial impact on sleep, daily activities and quality of life.
For the study, researchers questioned 65,554 women and 23,119 men, all of whom were health professionals who took part in the Health Professionals Follow-Up Study or the Nurses’ Health Study II. None of the participants had diabetes, arthritis or were pregnant. Of the groups, 6.4 percent of the women and 4.1 percent of the men were identified as having RLS.
The research found men and women with a body mass index (BMI) score over 30 were nearly one-and-a-half times more likely to have RLS than people who were not obese.
In addition, people who were in the top 20 percent of the group for highest waist circumference were more than one-and-a-half times more likely to have RLS than the bottom 20 percent of the group with the lowest belly size. The results were the same regardless of age, smoking, use of antidepressants or anxiety.
“These results may be important since obesity is a modifiable risk factor that is becoming increasingly common in the U.S.,” said study author Xiang Gao. “More research is needed to confirm whether obesity causes RLS and whether keeping a low BMI score and small waist size could help prevent RLS.”
Gao says some studies suggest that obese people have lower dopamine receptor levels in the brain. “Since decreased dopamine function is believed to play a critical role in RLS as well, this could be the link between the two.” Dopamine is a chemical naturally produced by the body that transmits signals between nerve cells.
MEDICA.de; Source: American Academy of Neurology (AAN)
This source that you mention at the bottom here, is that where you found all this, or did you write most of this yourself? This is huge. All the information I have been finding about carbs being at the root of the obesity problem tend to point to diet again as a serious contender for the cause of RLS. I will post a short quote one more time about the deleterious effects of what we call wheat: From Wheat Belly by Wm Davis, MD: "While it remains a topic of debate, a substantial proportion of children and adults with attention deficit/hyperactivity disorder (ADHD) may also respond to elimination of wheat... It is unlikely that wheat exposure was the initial cause of autism or ADHD but, as with schizophrenia, wheat appears to be associated with worsening of the symptoms characterisic of the conditions... Wheat, in fact, nearly stands alone as a food with potent central nervous system effects. Outside of intoxicants such as ethanol... wheat is one of the few foods that can alter behavior, induce pleasurable effects, and generate a wihdrawal syndrome upon its removal."
Though dopamine receptors are not mentioned specifically in here, it looks to me like a connection can be made. Our food supply is most definitely tainted one way or another. And wheat is in almost everything except the produce aisle and the meat counter!
Yes, of course, wheat is well worth eliminating, along with dairy and sugar. We can discuss the foreign and hard to digest nature of these substances (especially gluten, casein) in terms of the adult gut and I've always believed these to underlie Crohn's Disease and UC, but like you said, we become addicted to them. Then begins that whole long article that I posted above and how these things if eaten everyday in large enough quantities will lead to the down regulation of our receptors, just like the agonists.
There must be a genetic reason for some to have RLS. My mother who was well built and her 9 sister none of which were obese and 4 were downright skinny, all had severe RLS. My weight to height ratio has always been within guidelines and I have suffered severe RLS for more than 40 years.
After reading the long article I may go on a starvation diet and exercise 3 times a day---lol
Yes, why not? I'm with you. Weight has nothing to do with it. I know people who can pack it away and never gain an ounce. And as long as your stomach is empty why not pop ONE iron pill, Windwalker? The littlest thing can trigger RLS (one anti-histamine) so it makes sense that the littlest thing should ease it too. Just make sure that iron gets to your brain and doesn't stay in your gut. Like MikeMan suggests, look on Amazon. Find a bio-available one. Then do a tonic water and potassium chaser and post here in the morning.
Like I said in another post, I'm looking for the lazy woman's way to up-regulated receptors. But for now, under-eating and anaerobic exercise is the only thing...if you're a mouse
Windwalker, here's a lazy person's way to upregulated receptors. It's short. But I would still scroll down to where it talks about Uridine Monophosphate and enhanced receptors.
corpina.com/uridine-supplem...
I want a short list of thing available in the drug store and not too many facts. I read the whole article and got a headache learning what mice like. KISS (keep it simple stupid)
Just a simple list.
There is NO simple list to keep it at the KISS level. Different countries have different products. Are you in the US or the UK or elsewhere, and this would also be better on a new post, it will only get buried here in this thread. make a new post and I will try and help. But there is NO easy over the counter list in ANY country.
Hi Windwalker, per this forum and research:
1. iron with vitamin c on empty stomach (ask Sarasneaker) or iron-bisglycinate from Amazon called "Easy Iron." $10
***ONLY AT NIGHT OR DURING AN ATTACK***
If it works for you, as it did for Sara, then talk to your doctor about it.
2. Potassium Citrate (take as per bottle) or cream of tartar - 1/2 to 3/4 teaspoon in water. Saw it on this forum then googled it and found out it is the residue from inside wine barrels and pure potassium tartrate. So citrate or tartrate, your call, but I would try the tartrate first and only once. AND cream of tartar is the new miracle drug for a lot of conditions per internet alternative medicine gurus. $2.39 in grocery aisle.
****ONLY DURING AN ATTACK***
That's all I would buy. You'll be about $15 dollars poorer.
I saw recently on here that someone was taking curcurmin and when I put it in the search box above I saw mustard come up as well - one teaspoon in a cup of water. You probably already own this. Start with the iron, then potassium, then mustard.
Potassium in sufficient quantity will cause a release of dopamine just as amphetamines do, no questions asked. It seems that scientists use it ROUTINELY in experiments to MIMIC the human brain on methamphetamines. Then the point of the experiments is to see what will reverse the effects of an overdose of meth. I wish I could tell you to just eat bananas but I know that won't work, I'm sure they're giving those mice a boatload of potassium.
"INTERMITTENT FASTING" - seems that everyone on the internet knows that this upregulates our dopamine receptors except us - meaning the RLS world. Although now we do :). But there have been numerous people on this forum who have felt a benefit from a restrictive diet and/or an empty digestive tract. Fasting will probably not relieve your symptoms in 20 to 60 minutes as the above substances will...but should be a great long term treatment. Fasting does NOT mean no food. It means just enough to keep from having hunger PAINs or fainting. And I hope the foods you do eat while "fasting" include things like raw fruits and vegetables or steamed broccoli or one soft boiled egg in the morning. Intermittent means one to two days per week. If these articles are correct then you should feel an improvement" in your RLS after that first, two day fast.
You will be a pioneer if you do intermittent fasting. I did not see one person on the internet doing this for RLS. For mood, for addiction, yes.
how do you know no one does intermittent fasting? I do it for several gastric issues I have. pancreatitis for one and gastroparesis. I assume you know what those are.
Also, with the gastroparesis, food does not digest in my stomach, and comes back up the wrong way. I am constantly doing a bland diet. So, do not assume, since this is an RLS forum, that we do not deal with many other issues.
No I do not know a great deal about either condition I do know that with rare exception a bland diet helps no GI tract condition. That is if you mean tea and toast bland. I get heartburn I call it my moral compass. It keeps me in line. Everythingives me heartburn except raw vegetables and steamed ones. Raw food digests itself because of the enzymes. Your stomach small intestine and pancreas get a vacation when you eat something raw. Sounds like your gi tract needs a vacation.
The pancreas gets vacation when you are in the hospital and they put you on an IV for 2 days to redusce inflammation and then they out you on a soft diet. Raw veggies would have me double over in pain when having an attack,. It is even the same for dogs. The only way to calm down a pancreatitis attack is to "starve" it. That is a fact and I have been thru it several times, THAT I do know about, at least you admit that you have little knowledge about this, for once.
What's soft on the outside is hard on the inside. Wonder bread, twinkies low fat milk , yoghurt, tofu, even beans lentils are so frickin hard to digest I want to scream my head off when I hear people say these things are good for digestive ills. If you eat a slice of apple you're hungry again in about ten minutes. Same is true for celery carrot arugula berries sprouts. That is how we ate since the dawn of mankind about a million years ago. We weren't great hunters until much later so even raw meat was not a daily component of our diet. Most fruits were an exotic so they too were not a big part of our diet. You're bucking up against a million years of evolution. It's only in the last few thousand years that "soft" foods came on the scene. I believe it takes a hundred thousand years for an adaptation to occur. Our pancreas' need about another 95,000 years before they"ll be able to thrive on processed foods. Good luck with your soft diet.
Well, it is working. I fasted all night and all day, water only, and have only eaten yogurt today, and guess what, hardly any pain! My soft diet is doing fine thank you very much. I have done this many times, so I guess I have adapted. Do you have any digestive issues or are you just quoting yet another thing that you have read somewhere? The info I supplied is from the Mayo Clinic, by the way. FYI have a great night! Do you live in the UK or elsewhere? Just wondering what time zone you are in.
Mayo Clinic emphasizes FRESH fruits and vegetables for pancreatitis. Of course they do, they have to. Raw fruits and vegetables digest themselves as long as they are fresh and raw or lightly steamed. Any food that digests itself will give your pancreas a rest. Actually all foods, including animals, if eaten raw, will digest themselves. Within each plant and animal are enzymes that start to break its cells down upon death or ingestion. Life eats life. Mother nature intended it to be this way. And she made provision for it. As long as you don't process those enzymes out you're home free. Your pancreas will barely have to work a day in it's life. Probably why there are so many digestive ills, the pancreas has gotten lazy over the eons and now we're asking it to produce enzymes for every single piece of food we put in our mouths. Another example is Eskimos. Non-eskimos and people in general who do not consume large quantities of Omega 3 (ie fish) have (might have) the ability to convert Omega 6 into Omega 3. We Americans ingest a lot more Omega 6 than Omega 3. Anyways, Eskimos' digestive tracts have no ability whatsoever to convert Omega 6 into Omega 3 because they consume so much Omega 3 that over the eons they lost the enzyme that does this. Same is true with our pancreas. It is not yet ready to keep up with the enzyme demand placed upon it by our processed foods devoid of enzymes. Well here's what Mayo says:
Lifestyle and home remedies
By Mayo Clinic Staff
Digestive Health
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Once you leave the hospital, you can take steps to continue your recovery from pancreatitis, such as:
•Stop drinking alcohol. If you're unable to stop drinking alcohol on your own, ask your doctor for help. Your doctor can refer you to local programs to help you stop drinking.
•Stop smoking. If you smoke, quit. If you don't smoke, don't start. If you can't quit on your own, ask your doctor for help. Medications and counseling can help you stop smoking.
•Choose a low-fat diet. Choose a diet that limits fat and emphasizes fresh fruits and vegetables, whole grains, and lean protein.
•Drink more fluids. Pancreatitis can cause dehydration, so drink more fluids throughout the day. It may help to keep a water bottle or glass of water with you.
No where in here does it talk about "soft" foods. Quite the opposite, vegetables and WHOLE grains are very hard...on the outside...but very soft on our digestive tract.
The point HERE is "AFTER" you leave the hospital. This is MY experience, so just stop please. I know what my doctors say and what works for ME. You do not have pancreatitis, so stop telling me how to treat it please. It is REAL pain, and it is one thing I do not need. Thank you and have lovely day!
The genes for RLS were discovered and named in 2004 and 2007. In my family alone, me, my 2 sisters, my 2 nieces, my mother, my oldest niece's kids who are 8 and 11 ALL have RLS and PLMD. The knowledge of RLS genetics have been around for lot of years. primary RLS and YES, there is such a thing as PRIMARY and SECONDARY RLS, GoFish. I have said this many times, and it is scientific RLS fact, not a "horse and buggy theory". 70% of ALL RLS is hereditary (genetic) I know way more "skinny" RLSer's than I know obese or overweight ones in my 5,000 members. Theories abound, but the genes are found, named and that cannot be argued. A gene is a gene is a gene, and it is easily "googled". Just put "Primary RLS" in your search engine.
I knew it was genetic when I saw my mom and 9 of her sisters all have it. The passage on to heirs is almost certain when all the woman in a family has it.
She will be protected if only one of her ''x'' chromosomes is defective and the hit or miss factor would cause some of the women to miss if all the ''x'' es were not defective in the same way, from good old dad and mom. I tried all the home remedies and have found the chemical meds marketed commercially, Maripex, Requip and the others and some gabapentin with a little vicodin are my only chance to sleep some and retain some sanity. Thanks for the comment.
Windwalker
Did someone ask you to leave?
Reprehensible isn't it. The man has served this country with his life. Yikes, you are the dopamine receptor woman!!! You should be awarded the Nobel Peace Prize for bringing that information to this forum. Xx Everyone is getting better...see for yourself.
How can you possibly say that everyone is getting "better". Do you mean all of us with RLS are getting better, because that is not clear to me at all. Some ARE after med changes, diet changes, remembering we are all different with different triggers. I have studied dopamine receptors for years, and there is a lot to it. I will give you that.
You should share the results of your studies. The scientific community's knowledge and understanding of RLS is profound. RLS isn't the great and powerful wizard of Oz that you are making it out to be, it's just a pathetic old man behind a curtain and science has pulled that curtain back. We have lackluster dopamine receptors because iron passes out of our brains the way water does a hole in a bucket. And our receptors desperately need that now you see it, now you don't, iron.
Let's pretend I have Crohns Disease and I'm in pain. My GI doctor will NEVER prescribe long term pain killers because he knows it's like pouring gasoline on fire and the pain will only be relieved for a few hours a day anyways. But there was a day and a time when gasoline was prescribed for CD. One day doctors will no longer prescribe pain killers and dopamine agonists for RLS because these substances just fan the flames.
What I'm saying is, that day is here. Heck lady, I counted five people on this forum alone, in one weeks time, that employed one of the following - treating/stopping their RLS trigger, gave their brains some iron, up-regulated their receptors through diet, exercise and other substances.
Mark my words, the days of down regulating our receptors through agonists and pain killers are nearly over.
I respectfully disagree on the pain meds. They do not "fan the flames" nearly as much as the dopamine meds do. Augmentation from dopamine meds is a daily issue in all 6 of my groups that I manage. It has been for years and years. The researchers that are front and center on RLS research, are saying now that they DO have to get away from the dopamine theory, saying also that they know they have to steer new studies in a different direction/directions. And that includes Johns Hopkins and also the Mayo Clinic and other international ones. Dopamine meds eventually DO feed the fire when used at the ridiculously high doses that are being used by some doctors that just do not know better and do not take the time to know better, resulting in total torture for their RLS patients. I call it cruel and inhumane treatment, and there are other examples, such as the 'cold turkey withdrawal" from dopamine meds. There is no reason for it, and it goes totally against the Hypocratic oath. This is directly aimed at one doctor from Johns Hopkins in the US. "First Do No Harm".
Why? Get it all out of you so you feel better - go ahead -
The dopamine receptor means quite a lot if you think deeply about
that one. Careful or you'll give yourself away..
What a shame because you have such good information about RLS
and obviously you are very intelligent - why not use it for good to help
the dear good people on here who are suffering including me with RLS?
A few gold coins if I could toss them to to you to not cause any more
drama on here - you know I would offer my grandkids gold coins to
for their college fund to not stir up trouble at times.. it works.
Yes, you're right, I don't care if people know that I have a soft spot for our armed forces. I didn't mean to take sides with the other day's drama or continue it today, but just as people feel loyalty to certain individuals, I feel loyalty to our men and women on the front lines.
Mt father was WWII vet whose plane was shot down behind German lines on D-DAY. 3 purple hearts, Bronze Star for Bravery, and so on. over 40 medals I have in the collection. So, I do have soft spot for veterans as everyone should. What that has to do with being totally disrespectful to certain members in the RLS SUPPORT GROUP is beyond me. Veterans, as well as civilians of ANY country should be treated with respect simply because we all suffer from the same disorder. MY 2nd passion, besides RLS, is WWII history, so please do not lecture on that subject. The idea is we all have RLS, all have our own opinions and FACTS on RLS. Respect should go across the board. I think what I think and what I know after 18 years of managing RLS support groups and one for other sleep disorders. You think what you think and that is it. EVERYONE of us will NEVER agree on everything until science catches up to all of the theories out there. But when presented with facts I really hope everyone keeps an open mind. There are some facts that cannot be ignored. BUT, this comment from me is about respect and a few instances lately have shown that everyone does not look at that word the same way and have shown it in a very disrespectful way. The "powers" that be have removed the vile and disgusting stuff, the worst stuff I have ever seen on this site, thankfully it is gone. It takes LOT to shock me, It got removed fast, within 6 or 7 hrs, so you may have missed the WORST lack of respect I have ever witnessed in a SUPPORT group, GoFish. I am going to assume you did NOT see it, so am giving you a pass here for now in this one subject. Again, my opinion, and what happened should NEVER happen in this setting.
I googled "upregulate d2 receptors" and found mostly forums. Here's an interesting one with loads of egghead info that needs to be sorted through for the rest of us. GoFish, are you game?? longecity.org/forum/topic/5...
I actually quite like that site. I will have a look at it. But before I do I bet I came across it too! I was looking for "the lazy man's" way to up-regulate. Sounds like there's a substance in breast milk and that they add to baby formula, called Uridine 5 Monophosphate (something like that) that not only causes a release of dopamine but will also up-regulate receptors. I know, sounds impossible. Substances that release dopamine (like cocaine) down-regulate our receptors. But leave it to mother nature to find a substance that will calm babies, have no side effects and even be healthful to our receptors. It's on my Amazon list 29
Where do I find your "Amazon" list?
Have to ask Mikeman, not my list.
oh THAT, never mind