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1. Nerves Keeping You Awake? Get Help Sleeping
2. What is Insulin Resistance and how does it affect your body?
3. Modern medicine discovers that a strong immune system really does cure colds, and the flu (from 2016)
4. The Chemical Imbalance Theory of Depression Debunked

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Nerves Keeping You Awake? Get Help Sleeping!

Sometimes the sensation (burning, coldness, numbness, tingling or pain) from your nerves can keep you up at night.

If you are having trouble falling asleep or staying asleep, there is a safe and effective way to help your body get the sleep you need on a daily basis, and it's not a drug.

Passion flower, just one of the ingredients in the RHP Sleep Support Formula, is widely used by herbalists and natural health practitioners around the world.

Passion flower contains active ingredients that help to relieve anxiety, relax and calm the individual. This acts to reduce day-to-day stress that can often make it harder to get a good night'sleep.

The RHP Sleep Support Formula is specifically designed to support physical relaxation and calmness, to help you get a restful night's sleep, and it can be safely used as often as needed.

You can learn more and order the Sleep Support Formula

You can always call at 888 758-5590 or 818 252-1038

What is Insulin Resistance and how does it affect your body?

There are 17 million diabetics in the United States and 80 million more who are in some stage of insulin resistance. A diet high in carbohydrates and lack of nutrition are the two main factors in creating insulin resistance. Insulin resistance is a "pre-diabetic" condition, which, when it gets extreme, becomes type 2 diabetes. Below are two doctors clarifying how this condition develops and its effects on the body:

"When cells become resistant to insulin, the receptors on their surfaces designed to respond to insulin have begun to malfunction."

"It simply means that the receptors require more insulin to make them work properly in removing sugar from the blood. Whereas before they needed just a touch to lower it, now they need a continuous supply of excess insulin to keep blood sugar within normal range."

"As time goes by, blood sugar rises higher and stays up longer after the carbohydrate meal despite the enormous amount of insulin mustered to lower it. Bear in mind that were your doctor to check blood sugar during this stage of developing insulin resistance, your blood sugar would be perfectly normal. The major silent change taking place is the ever-growing quantity of insulin needed to keep it that way."

excerpted from Protein Power
by Doctors Michael and Mary Eades

"The liver becomes resistant first, then the muscle tissue, then the fat. What is the effect of insulin on the liver? It is to suppress the production of sugar by the liver.

"The sugar floating around in your body at any one time is the result of two things, the sugar that you have eaten and how much sugar your liver has made. When you wake up in the morning it is more of a reflection of how much sugar your liver has made. If your liver is listening to insulin properly it won't make much sugar in the middle of the night. If your liver is resistant, those brakes are lifted and your liver starts making a bunch of sugar so you wake up with a bunch of sugar.

"The next tissue to become resistant is the muscle tissue. What is the action of insulin in muscles? It allows your muscles to burn sugar for one thing. So if your muscles become resistant to insulin it can't burn that sugar that was just manufactured by the liver. So the liver is producing too much, the muscles can't burn it, and this raises your blood sugar.

"Well the fat cells become resistant, but not for a while. It is only after a while that they become resistant. It takes them longer. Liver first, muscle second, and then your fat cells.

"So for a while your fat cells retain their sensitivity. What is the action of insulin on your fat cells? To store that fat. It takes sugar and it stores it as fat. So until your fat cells become resistant you get fat, and that is what you see. As people become more and more insulin resistant, they get fat and their weight goes up.

"But eventually they plateau. They might plateau at three hundred pounds, two hundred and twenty pounds, one hundred and fifty pounds, but they will eventually plateau as the fat cells protect themselves and become insulin resistant.

"As all these major tissues, this massive body becomes resistant, your liver, muscles and fat, your pancreas is putting out more insulin to compensate, so you are hyperinsulinemic [having an abnormally high level of insulin in the blood] and you've got insulin floating around all the time.

"Insulin floating around in the blood causes a plaque build up. Insulin causes the blood to clot too readily. Insulin causes cells that accumulate fatty deposits. Every step of the way, insulin's got its fingers in it and is causing cardiovascular disease. It fills it with plaque, it constricts the arteries, it increases platelet adhesiveness and ability of the blood to coagulate [clot]. Any known cause of cardiovascular disease, insulin is a part of."

"If you want to know if insulin sensitivity can be restored to its original state, well, perhaps not to its original state, but you can restore it to the state of about a ten year old."

"You can increase sensitivity by diet and a lot of supplements."

excerpted from a talk at the Designs for Health Institute given by Dr. Ronald Rosedale, noted Diabetic Specialist

Medicine discovers that a strong immune system really does cure colds, and the flu (from 2016)

Researchers from the Laboratory of Molecular Biology in Cambridge, England, have made a fascinating new discovery about the way the body's immune system fights off infections. Contrary to popular belief within mainstream medicine, the body's natural antibodies are capable of fighting off a virus and killing it, even after the infection has entered cells -- and this phenomenon occurs naturally without the need for drug interventions.

Immune System

The Chemical Imbalance Theory of Depression DebunkedA Decisive Blow to the Serotonin Hypothesis of Depression

An exhaustive new review debunks the “chemical imbalance” theory of depression.

In July 2022, there was an explosion of media in response to the UK study published in Molecular Psychiatry that definitively proved the chemical imbalance theory of depression had no basis in science. Headline news ran internationally.

Here is a review Posted July 19, 2022 | Reviewed by Vanessa Lancaster in Pscychology Today

Author: Christopher Lane, Ph.D., is a Professor Emeritus of Medical Humanities at Northwestern University.

Online: Christopher Lane — Author Website

KEY POINTS

• Surveys indicate that 85-90 percent of the public believes low serotonin or a chemical imbalance causes depression
• Among 237 psychology students interviewed, 46 percent had heard the chemical imbalance explanation from a physician.
• The serotonin hypothesis has been challenged repeatedly and found wanting, even as it remains popular and influential.
• A comprehensive, well-powered, high-quality umbrella review now determines that the theory is “not empirically substantiated.”

Almost as soon as it was floated in 1965 by Harvard psychiatrist Joseph Schildkraut, the serotonin hypothesis of depression—reduced and simplified by pharma marketing to the “chemical imbalance” theory of depression and anxiety—has been subject to critical research and found wanting.

The poor standing of the hypothesis in the scientific literature, however, barely dented its afterlife in textbooks, across clinical and treatment settings, and on mental health apps and websites. Nor has it dispelled the continued use of the phrase as “shorthand” between doctors and patients and in everyday settings, including for quite different mental states and conditions.

The “Chemical Imbalance” Metaphor Takes Root

Revisiting the history of this controversy raises several still-relevant details. In December 2005, as advertising for SSRI antidepressants flooded American magazines, talk shows, and network TV, the result of multibillion-dollar campaigns pitched in this case directly to consumers, Florida-based professors and researchers Jeffrey Lacasse and Jonathan Leo asked pointedly in PLoS Medicine, “Are the claims made in SSRI advertising congruent with the scientific evidence?”

The answer in “Serotonin and Depression: A Disconnect Between the Advertisements and the Scientific Literature,” their well-researched article, was a resounding no. The resulting “incongruence,” they determined, was “remarkable and possibly unparalleled.”

Lacasse and Leo found repeated evidence that the U.S. Food and Drug Administration had approved the marketing of SSRIs with two phrases still heavily in the subjunctive—that depression “may be due to a serotonin deficiency” and that SSRI efficacy, “modestly” outcompeting placebo, was “presumed to be linked to potentiation of serotonergic activity.” However, the research itself could not identify the precise mechanism.

The FDA had accepted aspirational language that the drugs “help to restore the brain’s chemical balance” and “bring serotonin levels closer to normal,” even though both claims were, and remain, scientifically meaningless.

“There is no such thing as a scientifically established correct ‘balance’ of serotonin,” Lacasse and Leo cautioned more than a decade ago, joining numerous other experts then and now. Additionally, both aspirational claims rest on a hypothesis that follow-up studies would end up contradicting repeatedly. In short, both the hypothesis and the expensive marketing that pushed it into American living rooms rested on a hedge: “Scientists believe that it could be linked with an imbalance of a chemical in the brain called serotonin.”

A Multibillion-Dollar Error

The hedge proved highly effective, even though, as David Healy explained in 2015 in “Serotonin and Depression,” in the BMJ, in practice, it entailed embracing or tacitly accepting “the marketing of a myth.” Through further oversimplification, a revised metaphor of a “chemical imbalance” took root as folk wisdom for multiple, dissimilar conditions listed in the DSM.

Returning to the controversy in “Antidepressants and the Chemical Imbalance Theory of Depression” (2015), Lacasse and Leo found that while the marketing had shifted emphasis from “correcting imbalances” to “‘adjusting’ or ‘affecting’ neurotransmitter levels,” leading psychiatrists were if anything, more wedded to the “chemical imbalance” metaphor than before.

Some had taken to the airwaves to say that it simplified communication with their patients. Daniel Carlat, the editor of The Carlat Psychiatry Report, explained on National Public Radio when asked what we know about psychiatric medication:

We don’t know how the medications actually work in the brain…. I’ll often say something like the way Zoloft works, is, it increases the level of serotonin in your brain (or synapses, neurons) and, presumably, the reason you’re depressed or anxious is that you have some sort of a deficiency. And I say that [chuckles] not because I really believe it, because I know the evidence really isn’t there for us to understand the mechanism—I think I say that because patients want to know something. And they want to know that we as physicians have some basic understanding of what we’re doing when we’re prescribing medications. They certainly don’t want to know that a psychiatrist essentially has no idea how these medications work (Qtd. in Lacasse and Leo).

The point in reproducing Carlat (who has made several such admissions on national media) was not to single him out but to stress how widespread the thinking and practice he shared so candidly. In 2007, as Lacasse and Leo pointed out, Frances, Lysaker, and Robinson found that among 237 psychology students interviewed, “46 percent had heard the chemical imbalance explanation from a physician.”

Inevitably, the problem of spreading false scientific information dovetails with that of medical ethics and the risk of enabling medically-induced harms. Because physicians swear to uphold the Hippocratic oath Primum non nocere (“First Do No Harm”), Lacasse and Leo questioned “the ethics of telling a falsehood to patients because you think it is good for them.”

They asked more broadly of those repeating the discredited hypothesis, whether as metaphor or oversimplification: “Do you believe it is ethical to present a falsified scientific theory as a fact to a patient? What are the possible negative effects of doing so?”

A significant consequence they anticipated at the time was that patients would realistically “conclude that they have been misled.”

Cut to the Present-day

A major new review of the research—the first of its kind exhaustively reviewing the evidence, published today in the journal Molecular Psychiatry—reaches a strikingly similar conclusion. In “The Serotonin Theory of Depression: A Systematic Umbrella Review of the Evidence,” University College London Psychiatry Professor Joanna Moncrieff and a team of five other top European researchers found “there is no evidence of a connection between reduced serotonin levels or activity and depression.”

The peer-reviewed umbrella review—representing one of the highest forms of evidence in scientific research—was extrapolated from meta-analyses and systematic reviews on depression and serotonin levels, receptors, and transporters involving tens of thousands of participants.

Although “the serotonin hypothesis of depression is still influential,” Moncrieff and coauthors noted, citing widely adopted textbooks published as recently as 2020 and surveys indicating that “85-90 percent of the public believes that depression is caused by low serotonin or a chemical imbalance,” the primary research indicates there is “no support for the hypothesis that depression is caused by lowered serotonin activity or concentrations.”

Among other key findings:

• “Research on serotonin receptors and the serotonin transporter, the protein targeted by most antidepressants, found weak and inconclusive evidence suggestive of higher levels of serotonin activity in people with depression.” Widespread use of antidepressants is seen as the likely cause.
• The researchers also looked at studies where serotonin levels had been “artificially lowered in hundreds of people” (by depriving their diets of the necessary amino acid that makes serotonin) and found that “lowering serotonin in this way did not produce depression in hundreds of healthy volunteers,” according to a 2007 meta-analysis and several recent studies.
• Numerous other reviews on re-examination were found to provide weak, inconsistent, or nonexistent evidence of a connection between serotonin and depression.
• The researchers also probed well-powered studies involving tens of thousands of patients that focused on gene variation, including the gene for the serotonin transporter. These found “no difference in the genes between people with depression and healthy controls.” As such, “high-quality genetic studies effectively exclude an association between genotypes related to the serotonin system and depression, including a proposed interaction with stress.”
• The researchers also looked at “the effects of stressful life events and found that these exerted a strong effect on people’s risk of becoming depressed—the more of these a person had experienced, the more likely they were to be depressed.”

Legacy Effects of a Discredited Theory

“The popularity of the chemical imbalance idea of depression has coincided with a huge increase in the use of antidepressants,” note Moncrieff and coauthor Mark A. Horowitz in the study’s press release. “Prescriptions for antidepressants have sky-rocketed since the 1990s, going from being rare to a situation now where one in six adults in England and 2 percent of teenagers are prescribed an antidepressant in a given year.”

The practical ramifications of the umbrella review are thus vast and consequential, involving millions of people across multiple countries because the findings are tied to a discredited theory that is still fueling mass prescribing on a global basis.

Moncrieff explained in the press release:

Patients should not be told that depression is caused by low serotonin or by a chemical imbalance and they should not be led to believe that antidepressants work by targeting these hypothetical and unproven abnormalities. In particular, the idea that antidepressants work in the same way as insulin for diabetes is completely misleading. We do not understand what antidepressants are doing to the brain exactly, and giving people this sort of misinformation prevents them from making an informed decision about whether to take antidepressants or not.

Invited to extrapolate the review’s findings for Psychology Today, Moncrieff added:

Antidepressant use has reached epidemic proportions across the world and is still rising, especially among young people. Many people who take them suffer side effects and withdrawal problems that can be really severe and debilitating. A major driver of this situation is the false belief that depression is due to a chemical imbalance. It is high time to inform the public that this belief is not grounded in science.

References

Frances CM, Lysaker PH, and Robinson RP. (2007) The “Chemical Imbalance” Explanation for Depression: Origins, Lay Endorsement, and Clinical Implications.” Professional Psychology: Research and Practice 38(4), 411-20. [Link]

Healy, D. (2015) Serotonin and Depression. BMJ 350, h1771 [Link]

Lacasse JR and Leo J. (2005) Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature. PLoS Medicine 2.12 e392. [Link]

Lacasse JR and Leo J. (2015) Antidepressants and the Chemical Imbalance Theory of Depression: A Reflection and Update on the Discourse (with Responses from Ronald Pies and Daniel Carlat). Behavior Therapist 38: 206-13 & 260-66. [Link]

Moncrieff J, Cooper RE, Stockmann T, Amendola S, Hengartner MP, and Horowitz, MA. (7.20.2022). “The Serotonin Theory of Depression: A Systematic Umbrella Review of the Evidence.” Molecular Psychiatry. DOI 10.1038/s41380-022-01661-0 [Link]

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