Hi Russ, thanks for all those links! You are absolutely right. Naltrexone (both high and low) will raise plasma endorphin levels. The only difference seems to be that a low dose will only cause a temporary blockade, so that the extra endorphins will be able to exert a biological effect. However high dose naltrexone, although raising plasma levels will block receptors. Thanks for explaining that to me.
Its true (but maybe slightly misleading?) to say that (high dose) naltrexone raises both endorphins & cortisol since although it raises endorphins it also blocks receptors (which is presumably what causes the cortisol to rise).
I expect LDN to lower cortisol (by raising endorphins) as you thought originally. Anecdotally that seems to be the case. Although according to this thread here at least there haven't been any studies done.
many thanks, garcia.
--- In infection-cortisol@yahoogroups.com, "Russ Farris" <russ@...> wrote: > > This abstract (http://cat.inist.fr/?aModele=afficheN&cpsidt=20242576) says: "Our previous studies have shown that repeated treatment with naltrexone, a nonselective opioid antagonist, results in increased plasma beta-endorphin levels." >
I think it is showing what happens to the beta-endorphin levels of heavy drinkers (pink curve) and normal drinkers (green curve) when they are given alcohol. Note that the alcohol raises the endorphin levels of the heavy drinkers and lowers the endorphin levels of the normal drinkers. I'm not sure what it all means yet, but it is so interesting that I thought I would pass it on.
I say "I think" this is what is happening because the information in the presentation is sketchy and I can't find any corresponding study by Gianoulakis et al. Russ www.potbellysyndrome.com
This abstract (http://cat.inist.fr/?aModele=afficheN&cpsidt=20242576) says: "Our previous studies have shown that repeated treatment with naltrexone, a nonselective opioid antagonist, results in increased plasma beta-endorphin levels."
This article (http://www.lowdosenaltrexone.org/ldn_and_ms.htm) says: "Naltrexone, when given to mice and people at high doses, raises endorphin levels in the body's effort to overcome the naltrexone blockade."
This article by Elaine Moore says: "Because LDN is known to increase the body’s levels of endogenous (produced naturally) endorphins, this therapy is particularly effective in treating disorders known as Endorphin-Deficiency states, including infertility. LDN is suspected of improving fertility both by stimulating endorphin production and by its beneficial effects on immune function."
I'm not sure who Steve Lambert is or what MEDDAC is, but I found this on a .mil site, and I have found them to be exceptionally worthwhile. Russ www.potbellysyndrome.com
Fitness Files - Naturally High By Steve Lambert MEDDAC-Japan
Exercise has shown to have many benefits. When you observe a fitness or training enthusiast, have you ever wondered why they have a terrific attitude and keen zest for life?
Most fitness enthusiasts can tell you about the “runners high.” The “runners high” is the pleasant feeling that goes along with a period of high exertion such as running, swimming, biking or a strenuous competitive sporting event.
Beta-Endorphin is a hormone that is produced by a small gland in the brain called the pituitary gland. This “endorphin” hormone is released in the blood and affects the nervous system in the brain and body to affect a perception of well being and in some cases has produced a sense of euphoria. Endorphins have been found to affect the body by helping it to return to a state of normal function. For example, if one has a temperature, endorphins assist in lowering the temperature. If one has a mild hyper-tension, the effect is to assist with lowering the blood pressure.
Endorphins have been found to influence many physiological and psychological functions. Endorphins assist in the release of growth hormone (GH) that is associated with muscle development following a hard workout. Endorphins affect appetite suppression, influence sleep patterns and are associated with increased immune functions, memory retention and learning.
The most renowned effects of endorphins include mood enhancement and pain modulation. Studies have shown that as a naturally-produced substance, endorphins are more effective than morphine in helping to suppress pain. Elevating your mood to provide a sense of well being is one of the major benefits attributed to endorphins. Endorphins will help to fight off stress-induced illnesses.
Exercise not only helps in building strong muscles and managing weight, but exercise also helps with the release of endorphins that benefit many physiological processes.
Cortisol seems to vary with beta-endorphin levels, and levels of both increase with treatment by naltrexone or the related drug, naloxone. Russ www.potbellysyndrome.com
This opiate-naltrexone-immunity business is so new to me, and it seems so important, that I've been looking for primers to give me the information I need to understand the PubMed abstracts. I'll post links to any particularly useful items I find, beginning with this one: http://teens.drugabuse.gov/mom/tg_opi2.php.
This short blurb was written for teenagers and gives a very concise introduction to the actions of opiates, including endorphins. Russ www.potbellysyndrome.com
After a year and a half, it looks like we've just had our first spam attack.
I've removed "helenyates23" from the group. Russ
----- Original Message -----
From: "helenyates23" <>
To: <infection-cortisol@yahoogroups.com>
Sent: Saturday, November 14, 2009 6:31 PM
Subject: [infection-cortisol] Re: The Deeply Discounted Grocery Program
Worked!!!
> Re: The Deeply Discounted Grocery Program Worked!!!
>
> I want to share this amazing tip that I just received about the programs
> at
Re: The Deeply Discounted Grocery Program Worked!!!
I want to share this amazing tip that I just received about the programs at
http://savingmorethanbefore.com I went to the supermarket with my neighbor
two weeks ago and she left with an overflowing cart of groceries and non food
items and to my shock only had to pay $ 23.36. She told me how she joined the
program at the website above. As soon as I got home I joined the program as
well. Last night I went shopping for Thanksgiving. We are having 12 people
over as we do every year. My grocery bill for this holiday has always been
in the neighborhood of $ 250.00. Thanks to this wonderful program this years
bill was only $ 31.19! I am so excited I want to share this wonderful program
with everyone I can! I have to say that their wholesale mall is equally great. I
have never seen so many name brand products at such ridiculously low prices. I
just finished my Christmas shopping and I can't help but smile thinking how
little I spent!
An LDN support group in Scotland is petitioning their Parliament to investigate and fund trails for Low Dose Naltrexone. Anyone may sign this petition, you do not have to be a resident.
Preclinical investigations in animals and clinical observations in patients with multiple sclerosis suggest an alteration of endogenous opioids in multiple sclerosis.
In this study, Dr. Zagon and his colleagues studied mice induced with EAE, a model often used in studies of MS. To understand the role of opioids, these mice were treated with high and low doses of naltrexone. High doses of naltrexone cause a sustained blockade of the opioid receptor, thereby reducing the body’s production of endogenous opioids. When low dose naltrexone (LDN) is given, the opioid receptor is blocked for 4-6 hours. During the 18-20 hours daily following the blockade, a supersensitive response occurs in which endogenous opioid production and production of opioid receptors are dramatically increased.
The recently completed Combination of Prescription Omega-3 With Simvastatin (COMBOS) study confirmed that prescription omega-3 fatty acid administered in combination with simvastatin achieves statistically significant improvements across a range of lipid indicators beyond the LDL primary target, including triglycerides, non-high-density lipoprotein cholesterol, and lipoprotein particle size. In conclusion, several classes of drugs, including omega-3 fatty acids, can be used in combination with statins to achieve more global improvements in lipid profiles.
I take it as a general rule that anything that suppresses the immune system promotes infection and/or cancer. Here is an apparent exception. Russ www.potbellysyndrome.com
Rheumatoid Arthritis Treatment Doesn't Promote Cancer
No added risk among patients taking immunosuppressants, research shows
HealthDay, By Robert Preidt, Thursday, October 29, 2009
THURSDAY, Oct. 29 (HealthDay News) -- Treatment with tumor necrosis factor (TNF) blockers doesn't increase rheumatoid arthritis patients' risk of cancer, new research has found.
TNF is a substance secreted by immune cells that regulates the immune system and plays a role in inflammation. TNF blockers are immunosuppressants that reduce inflammation in people with rheumatoid arthritis, but concerns have been raised that long-term use of the drugs may increase the risk of infections and cancer.
Swedish researchers analyzed data from 6,366 rheumatoid arthritis patients who started anti-TNF therapy with infliximab (Remicade), adalimumab (Humira) or etanercept (Enbrel) between January 1999 and July 2006. The study participants were compared with other groups of rheumatoid arthritis patients, including 61,160 not taking medications, 4,015 taking methotrexate (the gold standard of treatment) and 4,105 taking combinations of disease-modifying anti-rheumatic drugs (other than TNF blockers).
According to the study authors, 240 first cancers were diagnosed during follow-up among patients who had no history of cancer when they began anti-TNF treatment. Compared to rheumatoid arthritis patients who didn't take anti-TNF drugs or those with no history of cancer, the relative cancer risk of anti-TNF therapy was 1.00 and remained unchanged for those taking immunosuppressant drugs for up to six years, the researchers found.
"Our research indicates the overall cancer risk is the same for rheumatoid arthritis patients on immunosuppressant therapies and those not taking medications for the disease," confirmed team leader Dr. Johan Askling, of the Karolinska University Hospital in Stockholm, in a news release. However, "given several uncertainties, continued vigilance remains prudent."
The study is published in the November issue of Arthritis & Rheumatism.
Reuters Health, Thursday, October 29, 2009, By Joene Hendry
NEW YORK (Reuters Health) - Low vitamin D levels in the body may be deadly, according to a new study hinting that adults with lower, versus higher, blood levels of vitamin D may be more likely to die from heart disease or stroke.
Vitamin D is an essential vitamin mostly obtained from direct sunlight exposure, but also found in foods and multivitamins.
Dr. Annamari Kilkkinen, at the National Institute for Health and Welfare in Helsinki, Finland, and colleagues compared blood levels of vitamin D and deaths from heart disease or stroke over time in 2,817 men and 3,402 women in Finland.
At enrollment, participants were just over 49 years old on average, and had no indicators of cardiovascular disease, the researchers note in the American Journal of Epidemiology.
During follow-up of about 27 years on average, 640 of the participants (358 men) died from heart disease and another 293 (122 men) died from stroke.
Compared with participants' with the highest vitamin D, those with the lowest had 25 percent higher risk of dying from heart disease or stroke, Kilkkinen noted in an email to Reuters Health.
There was a "particularly striking association" between vitamin D levels and stroke deaths, the researcher noted, in that having the lowest vitamin D seemed to confer "twice the risk," compared with having the highest vitamin D.
Allowing for age, gender, and other demographic factors, plus alcohol intake, smoking, physical activity, and season in which vitamin D levels were obtained did not significantly alter these associations.
In this study, vitamin D levels were "substantially lower" than levels thought to be sufficient, and "somewhat lower" than those reported in previous studies in other European and American populations.
However, there is no "absolute consensus" as to what the optimal range of vitamin D should be, the investigators note. Also, it's not known whether low vitamin D actually causes increased risk for heart disease or stroke. Clearly, further study is needed, they conclude.
SOURCE: American Journal of Epidemiology, October 15, 2009
It has been speculated for a long time that the cardiovascular benefits of statins comes from their antimicrobial properties. Russ www.potbellysyndrome.com
Cholesterol Drugs May Help Prevent Flu Deaths
But expert says it could be that statins protect heart during infection
HealthDay, Thursday, October 29, 2009
THURSDAY, Oct. 29 (HealthDay News) -- Statins, frequently used to cut cholesterol levels, may also help prevent death from severe flu, a new study suggests.
According to the researchers, a growing body of evidence suggests that statins -- which include medicines such as Lipitor, Crestor and Zocor -- can reduce death from severe infections. Whether they help with flu, however, has been more uncertain.
"Statins may have a role in reducing mortality from influenza, but our findings do not justify broader use of statins without confirming these findings in the setting of randomized controlled trials," said study author Dr. Ann R. Thomas, from the Emerging Infections Program at the Oregon Department of Human Services Public Health Division in Portland.
"Statins may have a benefit, in conjunction with vaccine and antivirals, in reducing morbidity and mortality associated with influenza, likely due to their effect of reducing the body's inflammatory response to influenza infection," she added.
The results of the study are to be presented Friday at the Infectious Diseases Society of America annual meeting in Philadelphia.
For the study, Thomas' team looked at the outcomes of hospitalized influenza patients over two flu seasons.
The researchers found that patients who were taking statins were more likely to be older, male, white or Asian with underlying health conditions such as cardiovascular disease. In addition, they were more likely to have had a flu shot.
While those with cardiovascular disease were more likely to die, those who received statins while in the hospital were less likely to die.
Whether statins are also effective in preventing deaths from the H1N1 swine flu is not known, Thomas said. "Our data are from the 2007-2008 influenza season, well before novel H1N1 emerged, so no one knows for sure if statins would reduce mortality from H1N1," she said.
"However, since the likely mechanism of statins in reducing mortality is their general effect of down-regulating the immune system, it is plausible that statins might be useful in treating influenza infections due to novel H1N1," she noted.
Infectious diseases expert Dr. Marc Siegel, an associate professor of medicine at New York University School of Medicine in New York City, said that the study "is of limited value."
Siegel believes it's statins' ability to prevent death from heart disease and not any benefit against flu that results in fewer deaths among those taking these drugs.
"Influenza increases your risk of dying from heart disease. At the same time, statins reduce your risk of dying from heart disease. So, it's not surprising to find that there are fewer deaths among those taking statins," Siegel said.
"You can't conclude from this study that people with influenza should take statins," he said. "Statins are protective in a situation where the heart is at risk, even influenza -- that, I'll buy."
SOURCES: Ann R. Thomas, M.D., M.P.H., Emerging Infections Program, Oregon Department of Human Services Public Health Division, Portland; Marc Siegel, M.D., associate professor, medicine, New York University School of Medicine, New York City, and author, Swine Flu: The New Pandemic; Oct. 29, 2009, presentation, Infectious Diseases Society of America annual meeting, Philadelphia
Hi Garcia,
Thanks for the critique of my hypothesis. I'm still learning about
naltrexone, and will write more soon. Russ
----- Original Message -----
From: "Garcia" <jgarcia3788@...>
To: <infection-cortisol@yahoogroups.com>
Sent: Wednesday, November 11, 2009 4:10 AM
Subject: [infection-cortisol] Re: Cravings, cortisol, & naltrexone;
brain-storming
> Hi Russ,
> fascinating info. I think your original assumption is correct, that LDN
> boosts the immune system & lowers cortisol (the immune system boosting
> may be direct rather than as a result of cortisol lowering per se).
>
> It is true that naltrexone raises cortisol levels, but my understanding
> is that is because naltrexone and LDN (paradoxically) have opposite
> effects. Naltrexone causes an opioid blockade on the body, so will block
> the body's endogenous supply of opioids. Opioids get sent to zero, and
> cortisol rises.
>
> With the LDN there is merely a temporary blockade on the opioid
> receptors. The body responds by increasing its own endogenous supply. In
> other words naltrexone lowers opioids, but LDN raises opioids. So if we
> know (e.g. from pubmed studies) that Naltrexone (blocks opiods &) raises
> cortisol, it is entirely consistent that LDN (increases opiods &) lowers
> cortisol.
>
> Could that explain the paradox?
>
> garcia.
>
>
> --- In infection-cortisol@yahoogroups.com, "Russ Farris" <russ@...>
> wrote:
>>
>> This is a long account of the reading and brainstorming I've been
> doing since Garcia and Yannic got me interested in low-dose naltrexone
> (LDN) last week.
>> I've been trying to find some mechanism that would explain the
> panacea-like effects that have been claimed for LDN. I assumed that LDN
> boosted immune system performance by lowering cortisol levels, but that
> doesn't seem to be the case. In fact, naltrexone appears to raise
> cortisol levels, although for how long, and under what circumstances,
> I'm not sure.
>> Tonight I came across the term cue-induced cortisol. Plugging
> that term into www.PubMed.gov got 10 hits, including the abstract
> below, which suggests that just thinking about alcohol raises cortisol
> levels in alcoholics.
>> In The Potbelly Syndrome (p. 119), we described a study by
> Mclean, Barr, and Prior that suggested that just thinking about food
> raises cortisol levels. That was kind of perplexing because I was pretty
> sure that it was the other way around, i.e., it was cortisol that made
> us think of food. But maybe not.
>> What if cravings--food, alcohol, cocaine, love, or
> whatever--raise our cortisol levels? What if cortisol actually helps us
> cope with cravings? There is a book called Rethinking Homeostasis that
> suggests that cortisol's main role is to help us deal with the outside
> world by making changes to our inner world. What if naltrexone raises
> our cortisol levels and the extra cortisol helps us cope with cravings,
> just as it helps us cope with other stresses? That's what appears to be
> happening.
>> The anecdotal and PubMed information on LDN suggests that it
> raises cortisol levels and boosts our immune systems. Cortisol, though,
> is a famous immune suppressor. I've been fretting for days trying to
> figure out this apparent paradox.
>> Here is a brief thought experiment. Naltrexone works by
> blocking opiod receptors. What if it also blocks cortisol receptors?
> That would produce cortisol resistance, and cortisol would not have its
> usual effects on cortisol-resistant cells, just as insulin doesn't have
> its usual effects on insulin-resistant cells.
>> If low-dose naltrexone makes immune cells cortisol resistant,
> this would raise blood cortisol levels just the way insulin resistance
> raises insulin levels. The extra cortisol wouldn't affect the
> cortisol-resistant immune cells, so they would continue to eat germs and
> kill cancer cells.
>> Not all kinds of cells become insulin resistant, and it's
> unlikely that all kinds of cells become cortisol resistant. Cells that
> remain cortisol-sensitive would be getting extra cortisol. Who knows
> what they are doing to or for people taking LDN?!
>> Is there any evidence that naltrexone makes cells cortisol
> resistant? Some. Cortisol makes liver and muscle cells insulin
> resistant. If naltrexone blocks cortisol receptors on liver and muscle
> cells, then we would expect naltrexone to reduce insulin resistance. And
> it does, at least in women with PCOS. Naltrexone has widespread and
> little-studied effects on the endocrine and immune systems.
>> I hope you all find this as interesting as I do. Russ
> www.potbellysyndrome.com
>> =========================
>> Alcohol Clin Exp Res. 2007 Mar;31(3):395-403.
>>
>> Stress-induced and alcohol cue-induced craving in recently abstinent
> alcohol-dependent individuals.
>> Fox HC, Bergquist KL, Hong KI, Sinha R.
>>
>> Department of Psychiatry, Yale University School of Medicine,
> Substance Abuse Center, Connecticut Mental Health Center, New Haven,
> Connecticut 06519, USA. helen.fox@...
>>
>> BACKGROUND: Research has shown that exposure to stress/negative affect
> and to alcohol cues can each increase alcohol craving and relapse
> susceptibility in alcohol-dependent individuals. However, whether the
> emotional and physiological states associated with stress-induced and
> alcohol cue-induced craving are comparable has not been well studied.
> Therefore, this study examined the craving, emotional, and physiological
> responses to stress and to alcohol cues in treatment-engaged, 4-week
> abstinent, alcohol-dependent individuals using analogous stress and
> alcohol cue imagery methods. METHOD: Twenty treatment-seeking,
> alcohol-dependent participants (18 males/2 females) were exposed to a
> brief 5-minute guided imagery procedure that involved imagining a recent
> personal stressful situation, a personal alcohol cue-related situation,
> and a neutral-relaxing situation, 1 imagery per session presented in
> random order. Alcohol craving, anxiety and emotion rating scales,
> cardiovascular measures, and salivary cortisol were compared across the
> 3 conditions. RESULTS: Exposure to stress and to alcohol cues each
> produced significant increases in alcohol craving, anxiety, and negative
> emotions and decreases in positive emotions. Stress-induced alcohol
> craving was significantly correlated with increases in sadness, anger,
> and anxiety ratings, but alcohol cue-induced craving was associated with
> decreases in positive affect (joy and neutral relaxed state) and
> increases in anxiety and fear ratings. Furthermore, stress increased
> systolic and diastolic blood pressure responses, but significant
> increases in salivary cortisol were only observed in the alcohol cue
> condition. CONCLUSIONS: Although both stress and alcohol cues produce
> increases in anxiety associated with alcohol craving, each produced a
> dissociable psychobiological state involving subjective emotional,
> cardiovascular, and cortisol responses. These data could have
> significant implications for understanding the specific psychobiology
> associated with stress or alcohol cue exposure and their potential
> effects on alcohol relapse susceptibility.
>>
>> PMID: 17295723
>>
>> http://www.ncbi.nlm.nih.gov/pubmed/17295723?
>>
>
>
>
>
> ------------------------------------
>
> Yahoo! Groups Links
>
>
>
There could be several reasons why some people may want to make their own LDN: Often their Doctors will not prescribe LDN; Homemade LDN costs only $10/month; There are no Pharmacy mistakes in Homemade LDN; There are no capsule "filler" problems and experiments can be conducted with different dose quantities.
There could be several reasons why some people may want to make their own LDN: Often their Doctors will not prescribe LDN; Homemade LDN costs only $10/month; There are no Pharmacy mistakes in Homemade LDN; There are no capsule "filler" problems and experiments can be conducted with different dose quantities.
The chemical we call Naltrexone is really the chemical Naltrexone Hydrochloride (C20H23NO4-HCl). It could be purchased directly from Spectrum Chemicals for about $100 a gram but only by using a commercial account and in its pure form is too difficult to measure in exact small quantities. The best source of Naltrexone, in order to prepare Homemade LDN doses, is the 50mg "ReVia" Naltrexone tablet made by DuPont and prescribed by Doctors for treatment of drug and alcohol addictions. Each 50mg "ReVia" Naltrexone tablet can be made into 11 to 16 LDN doses depending on whether one takes a small 3mg dose or a larger 4.5mg dose.
Hi Russ,
fascinating info. I think your original assumption is correct, that LDN
boosts the immune system & lowers cortisol (the immune system boosting
may be direct rather than as a result of cortisol lowering per se).
It is true that naltrexone raises cortisol levels, but my understanding
is that is because naltrexone and LDN (paradoxically) have opposite
effects. Naltrexone causes an opioid blockade on the body, so will block
the body's endogenous supply of opioids. Opioids get sent to zero, and
cortisol rises.
With the LDN there is merely a temporary blockade on the opioid
receptors. The body responds by increasing its own endogenous supply. In
other words naltrexone lowers opioids, but LDN raises opioids. So if we
know (e.g. from pubmed studies) that Naltrexone (blocks opiods &) raises
cortisol, it is entirely consistent that LDN (increases opiods &) lowers
cortisol.
Could that explain the paradox?
garcia.
--- In infection-cortisol@yahoogroups.com, "Russ Farris" <russ@...>
wrote:
>
> This is a long account of the reading and brainstorming I've been
doing since Garcia and Yannic got me interested in low-dose naltrexone
(LDN) last week.
> I've been trying to find some mechanism that would explain the
panacea-like effects that have been claimed for LDN. I assumed that LDN
boosted immune system performance by lowering cortisol levels, but that
doesn't seem to be the case. In fact, naltrexone appears to raise
cortisol levels, although for how long, and under what circumstances,
I'm not sure.
> Tonight I came across the term cue-induced cortisol. Plugging
that term into www.PubMed.gov got 10 hits, including the abstract
below, which suggests that just thinking about alcohol raises cortisol
levels in alcoholics.
> In The Potbelly Syndrome (p. 119), we described a study by
Mclean, Barr, and Prior that suggested that just thinking about food
raises cortisol levels. That was kind of perplexing because I was pretty
sure that it was the other way around, i.e., it was cortisol that made
us think of food. But maybe not.
> What if cravings--food, alcohol, cocaine, love, or
whatever--raise our cortisol levels? What if cortisol actually helps us
cope with cravings? There is a book called Rethinking Homeostasis that
suggests that cortisol's main role is to help us deal with the outside
world by making changes to our inner world. What if naltrexone raises
our cortisol levels and the extra cortisol helps us cope with cravings,
just as it helps us cope with other stresses? That's what appears to be
happening.
> The anecdotal and PubMed information on LDN suggests that it
raises cortisol levels and boosts our immune systems. Cortisol, though,
is a famous immune suppressor. I've been fretting for days trying to
figure out this apparent paradox.
> Here is a brief thought experiment. Naltrexone works by
blocking opiod receptors. What if it also blocks cortisol receptors?
That would produce cortisol resistance, and cortisol would not have its
usual effects on cortisol-resistant cells, just as insulin doesn't have
its usual effects on insulin-resistant cells.
> If low-dose naltrexone makes immune cells cortisol resistant,
this would raise blood cortisol levels just the way insulin resistance
raises insulin levels. The extra cortisol wouldn't affect the
cortisol-resistant immune cells, so they would continue to eat germs and
kill cancer cells.
> Not all kinds of cells become insulin resistant, and it's
unlikely that all kinds of cells become cortisol resistant. Cells that
remain cortisol-sensitive would be getting extra cortisol. Who knows
what they are doing to or for people taking LDN?!
> Is there any evidence that naltrexone makes cells cortisol
resistant? Some. Cortisol makes liver and muscle cells insulin
resistant. If naltrexone blocks cortisol receptors on liver and muscle
cells, then we would expect naltrexone to reduce insulin resistance. And
it does, at least in women with PCOS. Naltrexone has widespread and
little-studied effects on the endocrine and immune systems.
> I hope you all find this as interesting as I do. Russ
www.potbellysyndrome.com
> =========================
> Alcohol Clin Exp Res. 2007 Mar;31(3):395-403.
>
> Stress-induced and alcohol cue-induced craving in recently abstinent
alcohol-dependent individuals.
> Fox HC, Bergquist KL, Hong KI, Sinha R.
>
> Department of Psychiatry, Yale University School of Medicine,
Substance Abuse Center, Connecticut Mental Health Center, New Haven,
Connecticut 06519, USA. helen.fox@...
>
> BACKGROUND: Research has shown that exposure to stress/negative affect
and to alcohol cues can each increase alcohol craving and relapse
susceptibility in alcohol-dependent individuals. However, whether the
emotional and physiological states associated with stress-induced and
alcohol cue-induced craving are comparable has not been well studied.
Therefore, this study examined the craving, emotional, and physiological
responses to stress and to alcohol cues in treatment-engaged, 4-week
abstinent, alcohol-dependent individuals using analogous stress and
alcohol cue imagery methods. METHOD: Twenty treatment-seeking,
alcohol-dependent participants (18 males/2 females) were exposed to a
brief 5-minute guided imagery procedure that involved imagining a recent
personal stressful situation, a personal alcohol cue-related situation,
and a neutral-relaxing situation, 1 imagery per session presented in
random order. Alcohol craving, anxiety and emotion rating scales,
cardiovascular measures, and salivary cortisol were compared across the
3 conditions. RESULTS: Exposure to stress and to alcohol cues each
produced significant increases in alcohol craving, anxiety, and negative
emotions and decreases in positive emotions. Stress-induced alcohol
craving was significantly correlated with increases in sadness, anger,
and anxiety ratings, but alcohol cue-induced craving was associated with
decreases in positive affect (joy and neutral relaxed state) and
increases in anxiety and fear ratings. Furthermore, stress increased
systolic and diastolic blood pressure responses, but significant
increases in salivary cortisol were only observed in the alcohol cue
condition. CONCLUSIONS: Although both stress and alcohol cues produce
increases in anxiety associated with alcohol craving, each produced a
dissociable psychobiological state involving subjective emotional,
cardiovascular, and cortisol responses. These data could have
significant implications for understanding the specific psychobiology
associated with stress or alcohol cue exposure and their potential
effects on alcohol relapse susceptibility.
>
> PMID: 17295723
>
> http://www.ncbi.nlm.nih.gov/pubmed/17295723?
>
This is a long account of the reading and brainstorming I've been doing since Garcia and Yannic got me interested in low-dose naltrexone (LDN) last week.
I've been trying to find some mechanism that would explain the panacea-like effects that have been claimed for LDN. I assumed that LDN boosted immune system performance by lowering cortisol levels, but that doesn't seem to be the case. In fact, naltrexone appears to raise cortisol levels, although for how long, and under what circumstances, I'm not sure.
Tonight I came across the term cue-induced cortisol. Plugging that term into www.PubMed.gov got 10 hits, including the abstract below, which suggests that just thinking about alcohol raises cortisol levels in alcoholics.
In The Potbelly Syndrome (p. 119), we described a study by Mclean, Barr, and Prior that suggested that just thinking about food raises cortisol levels. That was kind of perplexing because I was pretty sure that it was the other way around, i.e., it was cortisol that made us think of food. But maybe not.
What if cravings--food, alcohol, cocaine, love, or whatever--raise our cortisol levels? What if cortisol actually helps us cope with cravings? There is a book called Rethinking Homeostasis that suggests that cortisol's main role is to help us deal with the outside world by making changes to our inner world. What if naltrexone raises our cortisol levels and the extra cortisol helps us cope with cravings, just as it helps us cope with other stresses? That's what appears to be happening.
The anecdotal and PubMed information on LDN suggests that it raises cortisol levels and boosts our immune systems. Cortisol, though, is a famous immune suppressor. I've been fretting for days trying to figure out this apparent paradox.
Here is a brief thought experiment. Naltrexone works by blocking opiod receptors. What if it also blocks cortisol receptors? That would produce cortisol resistance, and cortisol would not have its usual effects on cortisol-resistant cells, just as insulin doesn't have its usual effects on insulin-resistant cells.
If low-dose naltrexone makes immune cells cortisol resistant, this would raise blood cortisol levels just the way insulin resistance raises insulin levels. The extra cortisol wouldn't affect the cortisol-resistant immune cells, so they would continue to eat germs and kill cancer cells.
Not all kinds of cells become insulin resistant, and it's unlikely that all kinds of cells become cortisol resistant. Cells that remain cortisol-sensitive would be getting extra cortisol. Who knows what they are doing to or for people taking LDN?!
Is there any evidence that naltrexone makes cells cortisol resistant? Some. Cortisol makes liver and muscle cells insulin resistant. If naltrexone blocks cortisol receptors on liver and muscle cells, then we would expect naltrexone to reduce insulin resistance. And it does, at least in women with PCOS. Naltrexone has widespread and little-studied effects on the endocrine and immune systems.
Department of Psychiatry, Yale University School of Medicine, Substance Abuse Center, Connecticut Mental Health Center, New Haven, Connecticut 06519, USA. helen.fox@...
BACKGROUND: Research has shown that exposure to stress/negative affect and to alcohol cues can each increase alcohol craving and relapse susceptibility in alcohol-dependent individuals. However, whether the emotional and physiological states associated with stress-induced and alcohol cue-induced craving are comparable has not been well studied. Therefore, this study examined the craving, emotional, and physiological responses to stress and to alcohol cues in treatment-engaged, 4-week abstinent, alcohol-dependent individuals using analogous stress and alcohol cue imagery methods. METHOD: Twenty treatment-seeking, alcohol-dependent participants (18 males/2 females) were exposed to a brief 5-minute guided imagery procedure that involved imagining a recent personal stressful situation, a personal alcohol cue-related situation, and a neutral-relaxing situation, 1 imagery per session presented in random order. Alcohol craving, anxiety and emotion rating scales, cardiovascular measures, and salivary cortisol were compared across the 3 conditions. RESULTS: Exposure to stress and to alcohol cues each produced significant increases in alcohol craving, anxiety, and negative emotions and decreases in positive emotions. Stress-induced alcohol craving was significantly correlated with increases in sadness, anger, and anxiety ratings, but alcohol cue-induced craving was associated with decreases in positive affect (joy and neutral relaxed state) and increases in anxiety and fear ratings. Furthermore, stress increased systolic and diastolic blood pressure responses, but significant increases in salivary cortisol were only observed in the alcohol cue condition. CONCLUSIONS: Although both stress and alcohol cues produce increases in anxiety associated with alcohol craving, each produced a dissociable psychobiological state involving subjective emotional, cardiovascular, and cortisol responses. These data could have significant implications for understanding the specific psychobiology associated with stress or alcohol cue exposure and their potential effects on alcohol relapse susceptibility.
Its a fascinating interview not least because of the story Dr Berkson tells when he saved a couple of patients lives who had eaten poisonous mushrooms and were about to die of liver failure. He gave them IV Lipoic acid and they both survived against the odds. Dr Berkson was severely reprimanded over the incident for saving their lives when they were supposed to die!!
I'm currently reading the alpha lipoic acid breakthrough.
garcia.
--- In infection-cortisol@yahoogroups.com, "Russ Farris" <russ@...> wrote: > > Thanks, Yannic, for posting the interview with Dr. Berkson. He and my mentor Bernie Rimland were friends, and Bernie suggested that I contact Dr. Berkson about being a co-author of The Potbelly Syndrome. Dr. Berkson was too busy to work on the book, but he gave me a great deal of useful information and he encouraged me to keep plugging away at it. > Dr. Berkson's excellent book, The Alpha Lipoic Acid Breakthrough, convinced me that I should try alpha lipoic acid. I hope he writes a book about low-dose naltrexone. Russ www.potbellysyndrome.com > ----- Original Message ----- > From: Hen & Yan > To: infection-cortisol@yahoogroups.com > Sent: Sunday, November 08, 2009 1:28 AM > Subject: [infection-cortisol] Making headway against automimmune diseases with LDN > > http://www.63ok.com/health-fitness-blog/making-headway-against-autoimmune-diseases-with-low-dose-naltrexone/ > > Inner Circle interview with Burton Berkson, MD, PhD >
Thanks, Yannic, for posting the interview with Dr. Berkson. He and my mentor Bernie Rimland were friends, and Bernie suggested that I contact Dr. Berkson about being a co-author of The Potbelly Syndrome. Dr. Berkson was too busy to work on the book, but he gave me a great deal of useful information and he encouraged me to keep plugging away at it.
Dr. Berkson's excellent book, The Alpha Lipoic Acid Breakthrough, convinced me that I should try alpha lipoic acid. I hope he writes a book about low-dose naltrexone. Russ www.potbellysyndrome.com