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Following is an article from the Natural Medicine Journal: the journal of the American Naturopathic Association which provides an excellent review of the many clinical applications of Low Dose Naltrexone (LDN)

Reviewed applications include the following:

  • Anti-inflammatory activity
  • Regulation of the opioid growth factor
  • Autoimmune Conditions
  • Cancer
  • Depression
  • Dissociative Disorders and Post-Traumatic Stress Syndrome

As suggested in this review, LDN can provide an excellent therapeutic option for some of the health issues described.



The Uses of Low-Dose Naltrexone in Clinical Practice

Potential benefits for a wide range of conditions

By Timothy Schwaiger, ND, MA


The purpose of this paper is to review low-dose naltrexone (LDN) for use in clinical practice. The known or theoretical mechanism of action of LDN, clinical research findings in relation to various medical conditions including pain, autoimmune conditions, cancer, and mood disorders will be discussed. Recommended doses and forms of LDN will also be summarized.


Naltrexone, in oral form, was patented by Endo Laboratories in 1967 and approved by the US Food and Drug Administration (FDA) in 1984 for the treatment of opioid addiction.1 Referred to in early research as “ENDO1639A,” the drug would become what we know as naltrexone. In recent years, the use of buprenorphine and methadone have been recommended over naltrexone to reduce undesirable side effects and/or counter the effect of morphine partly due to lack of patient compliance with naltrexone.2

The use of oral naltrexone for opioid addiction requires detoxification from the opioid drug and has been associated with low adherence and high level of relapse back to opioid use after discontinuation of naltrexone.3,4 The typical daily oral dose of naltrexone is 50 mg but may vary depending on the addiction. An extended-release injectable naltrexone that only needs to be administered every 4 weeks is now available. This new method of naltrexone treatment produces better compliance rates in opioid-addicted individuals.5

Low-dose naltrexone was first used clinically in 1985 by Bernard Bihari, MD, a Harvard University physician and Director of the Division of Alcoholism and Drug Dependence, SUNY/Health Science Center at Brooklyn. He became the City Addiction Commissioner of New York in 1974 and continued working with drug addicts at the New York City Health Department and King’s County Hospital in Brooklyn, New York. Given his posts, he was steeped in the upcoming use of drugs such as methadone and naltrexone to treat addictions. He was aware of data indicating that naltrexone led to immune effects, an observation that was merely incidental to its approved use. In 1984, Bihari observed the therapeutic effects of the use of full-dose naltrexone (50 mg/dose) when given to heroin addicts. While naltrexone successfully blocked heroin’s ability to bind the opioid receptors, the complete blockage led to side effects so severe that the former addicts would not comply with continued use. Side effects such as severe anxiety, depression, irritability, and sleep disturbance hampered the adoption of naltrexone for long-term use.6

Meanwhile, while working for the Public Health Department in New York City in 1985, Bihari naturally became worried about the human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) epidemic that was surfacing. He turned his research attention and his knowledge of naltrexone’s effect on the immune system in that direction. Realizing that naltrexone’s effects included increasing endorphins—and that this raises immune competence—he began research into the use of naltrexone for the HIV-positive (HIV+)/AIDS population. He began with testing innate endorphin levels in individuals with HIV+/AIDS and found they were low in endorphin production compared to patients who did not have AIDS.7

Unlike higher doses of naltrexone, LDN acts on β-endorphin receptors to stimulate the release of endorphins in the body.

In an effort to find the minimal dose of naltrexone needed to raise endorphins, Bihari and his colleagues did a dose-ranging study comparing 50, 20, 10, 5 and 3.0 mg of naltrexone.6 They found that while all of these doses raised endorphins equally, a dose as low as 1.0 mg had no effect on endorphins. He then compared various doses of LDN between 1.75 and 4.5 mg and verified that a dose of 3.0 mg of LDN increased levels of endorphins during the night and even throughout the next day.8,9 At the International AIDS Conference in 1988 Bihari reported fewer opportunistic infections in a group of AIDS patients using LDN as compared to the placebo group. He also found a reduction in the level of interferon-alpha (IFN-α) in those taking the LDN.10 Increased levels of IFN-α have been implicated in comorbidities in HIV patients such as vascular and kidney disease.11 In addition, patients with HIV infections often have reduced levels of CD4+ T cells. Bihari found that CD4+ T cells did not decrease in patients who received LDN, compared to the placebo group (who were not treated with LDN). These findings and other clinical trials led to the approval of LDN in April 2016 for management of HIV patients in the country of Nigeria by the National Agency for Food and Drug Administration and Control (NAFDAC),12 Nigeria’s equivalent to the US Food and Drug Administration (FDA).

The FDA has not approved LDN for use for any medical conditions in the United States at doses below 5.0 mg, so it is only available from compounding pharmacies.

Mechanism of Action

Several mechanisms of action of LDN have been reported in the literature. The following are 3 of the most prominent actions of LDN: 1) action on opioid receptors to increase release of β-endorphins; 2) ability to reduce pro-inflammatory cytokines and increase anti-inflammatory cytokines; and 3) regulation of the opioid growth factor (OGF)/opioid growth factor receptors (OGFr) axis.

Endorphin production and opioid receptor activation

Bihari stated in his research that endogenous endorphins were released in the body between 2:00 am and 4:00 am; however, other research has shown that beta (β)-endorphins are released in healthy adults between 4:00 am and 10:00 am.13 Beta-endorphins bind to mu (μ) opioid receptors. This interaction between β-endorphins and μ receptors is thought to be responsible for the analgesic effects in the body.14 The word endorphin comes from the term “endogenous morphine.” Endorphins are found in the human body originating from the amino acid L-tyrosine and the methyl group of L-methionine.15

Morphine, the drug, is the exogenous equivalent to our own endogenous opioids. Morphine is derived from the opium poppy plant Papaver somniferum and has been used for many years for its analgesic properties.16 Endogenous morphine has been found in the adrenal gland, and secretion from the liver has been shown to increase following physical stress such as sepsis and surgery.17-19 In addition to increased levels of endogenous morphine following physical stress, levels of anti-inflammatory cytokines are released as a response to stresses such as surgery.

As mentioned, naltrexone in higher doses is classified as an opioid receptor antagonist and blocks the receptors to counteract the side effects of medication like morphine. Higher doses of naltrexone have also been shown to blunt the release of endorphins following physical activity.20 Unlike higher doses of naltrexone, LDN acts on β-endorphin receptors to stimulate the release of endorphins in the body.21 Low-dose naltrexone is still considered an opioid receptor antagonist, but only for a short duration, and research has shown that LDN increases levels of endogenous opioids.22 In addition, LDN stimulates the body’s own production of endorphins, even after the LDN is no longer in the system. In a 2008 study, researchers found elevations in endorphins even 1 month after discontinuation of LDN doses of less than 5.0 mg.23 So, the analgesic effects attributed to LDN, in part at least, most likely come from its ability to stimulate β-endorphin release in the body.

Anti-inflammatory activity

The increase of β-endorphins to reduce pain levels is only one aspect of the use of LDN in pain management, especially when the source of the pain is related to an inflammatory process. It has been shown that LDN reduces inflammation by reducing multiple pro-inflammatory cytokines.24 Cytokines are chemical messengers, often made by immune cells, whose net effect can be to either increase or decrease immune function. The coordination of the immune system rests on the body’s ability to keep a balance between cytokines that promote inflammation and those that reduce it. Cytokines are produced by various cells in the body and are associated with the physiologic experience of pain.25 However, the cytokine system isn’t simple. For example, tumor necrosis factor alpha (TNF-α) is associated with both increased inflammation and neuroprotection when the body is presented with an insult such as nerve damage.26,27 Excess synthesis or upregulation of TNF-α is associated with certain conditions such as cerebral ischemia, Alzheimer’s disease, and atherosclerosis, and reducing levels of this cytokine may be of benefit in treatment.28,29

In an 8-week single-blinded pilot study using 4.5 mg of LDN each night, serum levels of numerous proinflammatory cytokines including interleukin (IL)-1, IL-2, IL-12, IL-18, interferon gamma (IFN-γ), granulocyte-macrophage colony-stimulating factor (GM-CSF), and TNF-α were significantly reduced when compared to baseline in patients suffering from fibromyalgia.30

Regulation of the opioid growth factor

Low-dose naltrexone has been shown to upregulate the OGF/OGFr axis. Opioid growth factor is an opioid peptide also known as [Met5]-enkephalin. The name was changed to OGF due to the association of [Met5]-enkephalin with growth and cell proliferation. Cell growth cycles are classified as G1 (before DNA synthesis), S (DNA synthesis), G2 (before mitosis), and M (mitosis or cell division). OGF has been found to delay the G1/S phase of cell growth.31,32 In addition, there is evidence that the OGF/OGFr axis pathway is involved in the regulation of tumor growth.33 The use of LDN to regulate this pathway is of interest in cancer research and in the treatment of neurodegenerative diseases such as multiple sclerosis.34,35 In addition, research has shown that cell proliferation is altered when OGF binds to the OGF receptors. When the OGF/OGFr axis pathway is upregulated, tumor growth may be decreased.36

The treatment of pain is a complex challenge and can benefit from an approach that includes attention to both biological and psychological aspects of a patient’s symptoms. Healthcare practitioners have multiple tools available when facing the challenge of pain management. Treating the symptoms of pain using LDN as a monotherapy does not always work; however, if the patient’s condition is highly inflammatory (eg, rheumatoid arthritis) using LDN can be extremely helpful by itself.37

Of course, the use of opioids in this country has risen to an unprecedented level. It was reported in 2016 that 90 individuals die of opioid overdose in this country each day.38 The model of using a low dose of an opioid antagonist such as LDN is paradoxical. The benefit of using LDN for pain management has its foundations in the ability of this formulation to increase endogenous endorphins and decrease pro-inflammatory cytokines.

There have been several published articles on the use of LDN in patients suffering from fibromyalgia. In a 2013 placebo-controlled, crossover pilot study involving 31 women with fibromyalgia, a 4.5 mg dose of LDN at bedtime reduced daily pain levels (P=0.016) and improved mood (P=0.039) and overall reported quality of life (P=0.045). In this study, neither sleep nor fatigue improved.39 However, in a study conducted in 2009 by the same researchers, the same dose of LDN reduced pain levels and improved symptoms of fatigue (P=0.008) and stress (P=0.003) in 10 women with fibromyalgia.40

Autoimmune Conditions

Some of the more prevalent autoimmune conditions conducive to LDN therapy include rheumatoid arthritis (RA) and inflammatory bowel disease (predominately Crohn’s disease). Many autoimmune conditions present quite a challenge to physicians. Based on the scientific literature, LDN can offer a good option for those seeking pain relief along with a low side effect profile for some autoimmune conditions.

Rheumatoid arthritis is an autoimmune condition characterized predominantly by joint pain. Although not always present, this condition is frequently associated with a positive rheumatoid factor (RF) and anticyclic citrullinated peptide (anti-CCP) antibodies. Proinflammatory cytokines such as TNF-α and some interleukins such as IL-1 are often associated with RA. Using TNF inhibitors has been an option for treatment; however, in patients for whom treatment is unsuccessful, researchers have found elevated T-helper type 17 (Th17) cells, which do not respond to this therapy.41 Inhibitors of TNF include medications such as adalimumab (Humira), etanercept (Enbrel), and infliximab (Remicade). Other options for treating RA include nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, steroids such as prednisone, disease-modifying antirheumatic drugs (DMARDs) like methotrexate, and biological agents like the TNF inhibitors. T-helper 17 cells are responsible for the production of IL-17, a proinflammatory cytokine. In general, Th1/Th17 type cells are considered pro-inflammatory and Th2/regulatory T cells (Tregs) are anti-inflammatory. T-helper 2 activity has been shown to be reduced in patients with RA.42 To further explore the effectiveness of LDN on inflammatory conditions, clinical trials are currently ongoing to study the effects of LDN on adults with osteoarthritis and inflammatory arthritis.43

Crohn’s disease is characterized by abdominal pain, severe diarrhea, fatigue, weight loss, and malnutrition. It is considered an autoimmune disease because of the presence of serum and mucosal autoantibodies acting against intestinal epithelial cells. Results from research using LDN on patients with Crohn’s Disease have been mixed. In a 2014 article published in the Cochrane Data Base of Systematic Reviews, the authors stated that there was “insufficient evidence to allow any firm conclusions regarding the efficacy and safety of LDN used to treat patients with active Crohn’s disease.”44 This conclusion was based on 2 cited studies in which there was a significant positive clinical response; however, according to the authors of the Cochrane review, the number of remissions was not significant. In the one study mentioned, 25% of the 12 pediatric patients studied achieved clinical remission and 67% had a significant positive response to LDN therapy. In reviewing the actual study, which was called a “pilot study,” the authors conceded that the small sample size was a weakness. Also of note, the dose of LDN was based on body weight (0.1 mg/kg, up to 4.5 mg) and not a standard dose (eg, 4.5 mg).45 An adult study of the use of LDN on 17 patients with Crohn’s disease showed a 67% remission rate and a significant improvement in Crohn’s Disease Activity Index (CDAI) scores. In addition, both erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were significantly reduced (P=0.03).46

Multiple sclerosis (MS) is an autoimmune disease that damages myelin, the protective sheath that covers nerve fibers. The most common type of MS is called relapsing-remitting because it cycles between periods of remission and active destruction. Because there is no cure for MS, the focus of treatment is to reduce inflammation and slow the progression of the disease. Corticosteroids are used to reduce inflammation and a class of drugs known as disease-modifying therapies (DMTs) is used to try to slow the progression. Disease-modifying therapies include interferon beta (IFNB) 1-a and 1-b, glatiramer acetate (GA), mitoxantrone, natalizumab, fingolimod, teriflunomide, dimethyl fumarate, and alemtuzumab.47,48 Researchers have found that a larger number of IL-17 cells are found in the cerebrospinal fluid of patients suffering from MS compared to other noninflammatory neurological diseases. The inflammatory role of IL-17 cells is also important in Parkinson’s Disease and Alzheimer’s Disease.49 In addition, TNF-α, IFN-γ, and IL-1b have been shown to play a major role in neurodegenerative conditions, including MS.27

A retrospective study published in 2016 reviewed medical records from patients with relapsing-remitting MS who used either LDN only or LDN with glatiramer acetate, over a 10-year period (2006-2015). The study compared 3 parameters between the groups: laboratory values (eg, kidney function, liver enzymes); time to walk a 25-foot course unassisted; and changes in the brain based on MRI. Researchers concluded that there was no significant difference in the group that was treated with LDN alone vs those using the combination of LDN and glatiramer acetate.50 Even though there was no difference between the 2 groups, the authors concluded that LDN should be considered when treating MS patients because of the low cost. The average annual cost of LDN is around $212 per patient, while the annual cost of DMTs ranges from $41,078 to $53,032 per patient.51


To this author’s knowledge, there have not been any randomized clinical trials on the use of LDN as a monotherapy, or adjunctive therapy, for the treatment of cancer. However, there have been case reports, theoretical research, and in vitro studies.52,53 An in vitro study of triple-negative breast cancer (TNBC) cells revealed that the OGF/OGFr axis is diminished in these tumor cells. Since enhancing this pathway has been shown to have an inhibitory effect on cancer cells, LDN, which upregulates the OGF/OGFr axis, may offer some benefit in treating cancer such as TNBC.33 Triple-negative breast cancer is usually a more aggressive type of breast cancer with a poor prognosis. Because the cancer does not respond to hormone-based therapies, LDN is worth investigating for viability as an adjunctive therapy for TNBC.

In an attempt to determine the effects of modulating the OGF/OGFrc axis on cancer outcomes, researchers at Penn State College of Medicine studied the effects of infused OGF on patients with advanced unresectable pancreatic cancer and found that OGF increased survival time and, in 2 cases, resolved liver metastases.54 Another study looked at the use of OGF in patients failing standard chemotherapy for pancreatic cancer. Patients who received OGF therapy had a threefold increase in survival time compared to those who did not receive OGF therapy. In addition, patients on OGF therapy had significantly elevated blood levels of enkephalin after a month of treatment.55 Because LDN upregulates the expression of OGF and OGFr, these same researchers are exploring the use of LDN in the treatment of ovarian, pancreatic, and other types of cancer.56 There have also been 2 published reports (in 2006 and 2009) of long-term survival using LDN and infused alpha-lipoic acid in patients suffering from pancreatic cancer.52,53

In a study published in 2016, researchers compared standard doses of naltrexone with LDN on various genes involved in cell turnover. They found that genes responsible for apoptosis were upregulated by LDN but not by standard doses of naltrexone.57 In an in vitro study using ovarian cancer cells, investigators were able to demonstrate that LDN inhibited tumor growth when used with the chemotherapeutic agent cisplatin.35


There are no clinical studies evaluating the effectiveness of LDN as a monotherapy for depression. LDN has been studied, however, in patients with a history of using dopamine-enhancing medication for depression with history of relapse. Many factors are involved in the relapsing of major depressive disorders, and trying to develop ways to prevent relapses is a challenge.58 In a small study of 12 individuals using dopamine-enhancing medications for depression, the addition of 1.0 mg of LDN 2 times a day for 3 weeks appeared to improve relapsing symptoms of depression. Scores on the Hamilton Depression Rating Scale fell, on average, from 21.2 (severe depression) to 11.7 (mild depression) in patients who were on LDN.59

Dissociative Disorders and Post-Traumatic Stress Syndrome

There is limited information, mostly from case studies, on the use of LDN for post-traumatic brain injury syndrome and post-traumatic stress syndrome. One published study looked at using 2.0 to 6.0 mg of LDN when working with individuals with a history of repetitive, prolonged childhood trauma such as sexual abuse or cruelty. According to the author of the study, Wiebke Pape, MD, most of the people suffered from dissociative disorder, which she described at the 2017 LDN conference as the act of “shutting down” or where the “brain goes blank.” Of the 12 inpatients studied with LDN, most reported favorable benefits of taking LDN, including better regulation of traumatic memories and reduction of self-destructive impulses.60,61

Dosing Recommendations and Methods of Delivery

The recommended dose of LDN is typically 0.5 mg at bedtime for several weeks, followed by 0.5 to 1.0 mg incremental increases over a 1- to 3-month period. When using LDN for pain management, a thorough patient evaluation prior to each dosage increase is important. A thorough medical history including medications, nutritional supplements, and herbal formulas must be obtained before any LDN prescription. The decision to prescribe LDN as an adjunct to chemotherapy or other molecular or biologic agents for cancer treatment should be a joint decision that involves the prescribing physician, the oncologist, and the patient.

If a patient is at the typical maximum dose of 4.5 mg and symptoms return, the clinician should consider reducing or discontinuing LDN for 1 to 2 weeks, then reinitiating medication at a lower dose and building back up to a maximum effective dosage. When inflammatory markers are used to diagnose or follow a patient’s progress (eg, ESR, CRP) it is important to track these levels and correlate them with changes in symptomatology.

Oral use

Capsules and tablets can be prepared in any prescribed dose but the most common is 0.5 to 4.5 mg, typically taken at bedtime. Be sure to ask the pharmacist what fillers are used because patients might be sensitive to such things as lactose. Also, the size of the capsule can vary from pharmacy to pharmacy and many patients prefer the smallest capsule available. Tablets are usually very small and well-tolerated by patients, but not all pharmacies distribute tablets. Liquids or sublingual preparations can be made for those who want or need to avoid using capsules or tablets. Typical solutions are a 1.0 mg LDN per 1.0 mL glycerol solution. Liquids are often preferred over capsules or tablets for young children, or adults with swallowing difficulties.

Most LDN is prescribed at bedtime; however, if patients report nightmares, then taking the dose in the morning can be an alternative. Vivid dreams are the most commonly reported side effect in clinical trials but this seems to decrease after a few nights. Another less common side effect is headaches, but these are reported as mild in severity. No side effects of stomach ulcers, renal impairment, or interference with anticlotting medications have been reported in research.62


Considering its low cost and low side effect profile, LDN in oral form has potential clinical utility in the treatment of a wide variety of conditions including inflammatory diseases, fibromyalgia, neurological conditions, cancer, and mood disorders.

About the Author

Timothy Schwaiger, ND, MA, received his naturopathic degree from Southwest College of Naturopathic Medicine in Tempe, Arizona, and completed a two-year residency there in Family Medicine. Schwaiger recently served as Chief Medical Officer at Bastyr University in California before moving to Prescott, Arizona with his wife, Debra.

Schwaiger has been in practice since 1999 and loves being a naturopathic physician. He uses naturopathic modalities as well as an integrative approach to family care, pain management and cancer therapy.


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  53. Berkson BM, Rubin DM, Berkson AJ. Revisiting the ALA/N (alpha-lipoic acid/low-dose naltrexone) protocol for people with metastatic and nonmetastatic pancreatic cancer: a report of 3 new cases. Integr Cancer Ther. 2009;8(4):416-422.
  54. Smith JP, Conter RL, Bingaman SI, et al. Treatment of advanced pancreatic cancer with opioid growth factor: phase I. Anticancer Drugs. 2004;15(3):203-209.
  55. Smith JP, Bingaman SI, Mauger DT, Harvey HH, Demers LM, Zagon IS. Opioid growth factor improves clinical benefit and survival in patients with advanced pancreatic cancer. Open Access J Clin Trials. 2010;2010(2):37-48.
  56. Donahue RN, McLaughlin PJ, Zagon IS. The opioid growth factor (OGF) and low dose naltrexone (LDN) suppress human ovarian cancer progression in mice. Gynecol Oncol. 2011;122(2):382-388.
  57. Liu WM, Scott KA, Dennis JL, Kaminska E, Levett AJ, Dalgleish AG. Naltrexone at low doses upregulates a unique gene expression not seen with normal doses: implications for its use in cancer therapy. Int J Oncol. 2016;49:793-802.
  58. Burcusa SL, Iacono WG. Risk for recurrence in depression. Clin Psychol Rev. 2007;27(8):959-985.
  59. Mischoulon D, Hylek L, Yeung AS, et al. Randomized, proof-of-concept trial of low dose naltrexone for patients with breakthrough symptoms of major depressive disorder on antidepressants. J Affect Disord. 2017;208:6-14.
  60. Pape W, Woller W. Low dose naltrexone in the treatment of dissociative symptoms [in German]. Nervenarzt. 2015;86(3):346-351.
  61. Pape W. A medication to stay in the present: treating dissociative symptoms in trauma-related disorders. LDN 2017 Conference. Portland, Oregon; September 22-24, 2017.
  62. Younger J, Parkitny L, McLain D. The use of low-dose naltrexone (LDN) as a novel anti-inflammatory treatment for chronic pain. Clin Rheumatol. 2014;33(4):451-459.

Robert Lamberton Consulting

Functional Medicine / Biological Age Reversal Consultant

Nutritional Therapy Practitioner (NTP)

Certified Light/Darkfield Microscopy Nutritionist

Product Formulator of Professional Nutraceutical Products

Author of the Biotics Research Educational Newsletter for Doctors  

Contributing Writer / Advisory Board Member:

Nutricula: The Science of Longevity Journal    

Healthy Organic Woman Magazine

Twitter: rob_lamberton

Skype: larch60 Facebook: rlamberton  

LinkedIn ID


Phone: 778-227-4952

You have probably heard "The Buzz" - researchers, health care 
practitioners and the general public are starting to gobble down 
Metformin for its (supposedly) magical anti-aging benefits.

Some even refer to it as: "Vitamin M".

But as we discuss in this edition of our newsletter, there is a dark 
side to Metformin.

I myself have never been a fan - and quite frankly I cannot see 
the rationale for using it when we have available such a fabulous 
range of medicinal herbs and a concentrate which provide berberine 
compounds which provide all the benefits of Metformin - in addition 
to some which Metformin does not (such as cardiovascular benefits)

Following is a great article by Chandler Marrs, PhD from the website:
Hormones Matter on this very topic.

In this article, she discusses in some detail some of the health 
issues that Metformin consumption can cause: 

Here is a summary of the main points she discusses - plus her 
concluding commentary:

Metformin and Vitamin B12 Deficiency

Metformin, Pregnancy and Maternal and Fetal Complications
Metformin Inhibits Exercise-Induced Insulin Sensitivity

Metformin and Mitochondrial Damage

Metformin Alters 

Immune Reactivity via the Mitochondria

Metformin and the Statins: Beware

Here is a summary of her comments:

My Two Cents

When we contrast the reduction in glucose mediated by Metformin with the damage this medication does to the mitochondria and immune signaling, along with its ability to leach vitamin B12, block insulin sensitivity and reduce aerobic capacity, one cannot help but wonder if we are causing more harm than good. Admittedly, obesity and hyperglycemia are growing problems in Western cultures. As we are coming to learn, however, obesity itself is not linked to the diseases processes for which many drugs like the statins and Metformin are promoted to protect against – obesity paradox. Growing evidence suggests that obesity is indicative of mitochondrial dysfunction and chemical exposures which then may provoke impaired insulin sensitivity and hyperglycemia and continued fat storage versus metabolism. If this is true, simply reducing circulating glucose concentrations, in an effort to reduce obesity and the purported health problems associated obesity, will do nothing to treat the underlying problem.

Insulin resistance and the associated hyperglycemia are environmental and lifestyle mediated problems that should be reversible with environmental and lifestyle changes. Having said that, those lifestyle and dietary changes will fail unless we consider the underlying mitochondrial damage initiated by dietary choices, pharmaceutical and other environmental exposures. For that we must dig deeper into mitochondrial functioning and correct what we can.

I believe obesity and hyperglycemia are symptoms of damaged and dysfunctional mitochondria, partly mediated by lifestyle, partly iatrogenic (pharmaceutically induced) and likely epigenetic. If we are to solve the ‘obesity’ problem and prevent the damage mediated by hyperglycemia, we have to address these variables. Failing to do so serves no one except those who profit from our continued ill-health.

Product Spotlight

Within our Cutting Edge Naturals product offering, we have available
a very high potency blood sugar/diabetes formulation.

We recently started shipping some of our formulations over to one of
the largest countries in Asia: a country in which the population has
a genetic predisposition towards blood sugar and diabetes problems
(there are currently over 200,000,000 individuals in the general 
population with blood sugar/diabetes issues).

We initially sent over enough inventory of our DiaBalance formulation
to get it into the hands of some 30 MD's - and after trying it with
patients for a month, 100 % wanted to access the formulation for their

The anecdotal feedback was very impressive: some of these MD's advised
their patients to stop taking their prescription diabetes meds and
start on our DiaBalance formulation (something I as a pratitioner 
would not do: I would titrate them). The feedback was that the 
transition went off without any side effects whatsoever.

Also some of the patients had been suffering from neuropathies for 
many years and many of them saw their pain disappear in as little 
as a week.

This formulation includes not only some of the conventional ingredients
that we in the west are familiar with, such as berberine, gymnema
sylvestre, chromium etc. - but also a couple of patented nutraceuticals:
InnoSlim and InSea2 plus several Rain Forest herbs such as Pedra Hume
Caa, Pata de Vaca and Chanca piedra all of which target specific aspects
of blood sugar balance - but they also target Aldose Reductase, which is
involved in causing some of the nerve damage so common in diabetes.

       Here is a link to a Product Profile on DiaBalance

In my opinion (which is backed by some published research) there are
safer - and arguably more effective alternatives to Metformin for 
blood sugar issues, brain health - and overall anti-aging benefits

Following is the article.


Rob Lamberton

Stop the Metformin Madness

I have never been a fan of Metformin. It seemed too good to be true. Many years ago I had a conversation with a researcher about all of its possible therapeutic indications. His lab was actively pursuing the anti-cancer angle. That should have been a clue that Metformin might be causing more damage than we recognized, but it wasn’t. At that point, I was still enamored with the wonders of pharmacology and hadn’t yet begun my path toward understanding medication adverse reactions. Indeed, it wasn’t until very recently, when a family member began suffering from one of these reactions, that I began my investigation in full. This is what I learned.

Type 2 Diabetes is Big Business

The global profits from Type 2 diabetes medications rested at a paltry $23 billion dollars in 2011 but are expected to grow to over $45 billion annually by 2020. The market growth is bolstered in large part by the ever-expanding demand for therapeutics like Metformin or Glucophage. Metformin is the first line of treatment and standard of care for insulin resistance across all populations of Type 2 diabetics with over 49 million Americans on Metformin in 2011-2012. It is particularly popular in women’s health with an increasing reliance on Metformin for the metabolic dysfunction observed in women with PCOS, PCOS-related infertility and even gestational diabetes. Metformin is prescribed so frequently and considered so innocuous that it is sometimes euphemistically referred to as vitamin M.

If we quickly scan the safety research for metformin, there is little immediate evidence suggesting any side effects whatsoever. In fact, in addition to controlling blood sugar by blocking the hepatic glucose dump, this drug is suggested to promote weight loss, increase ovulation in women, (thereby helping achieve pregnancy) and prevent an array of pregnancy complications (everything from miscarriage to gestational diabetes, pre-eclampsia  and preterm birth). Metformin is argued to prevent cancer and the neurocognitive declines associated with aging, even aging itself. By all accounts, Metformin is a wonder drug. Why isn’t everyone on Metformin prophylactically? Increasingly, we are.

With the increasing rates of obesity and associated metabolic disturbances, drugs that purportedly reduce those indicators are primed for growth. Like the push to expand statin prescription rates from 1 in 4 Americans to perhaps 1 in 3, millions have been spent increasing the therapeutic indications and reach for this medication. Amid all the excitement over this drug, one has to wonder if it isn’t too good to be true. In our exuberance to get something for nothing, to have cake, if you will, have we overlooked the very real risks and side effects associated with Metformin?  I think we have.

Metformin and Vitamin B12 Deficiency

As we’ve reported previously, Metformin leaches vitamin B12 and to a lesser degree B9 (folate) from the body. One study found almost 30% of Metformin users are vitamin B12 deficient. For the US alone, that’s almost 15 million people who could be vitamin B12 deficient and likely do not know that they are deficient. What happens when one is vitamin B12 deficient?

Firstly, inflammation increases, along with homocysteine concentrations, which is a very strong and independent risk factor for heart disease (the very same disease Metformin is promoted to prevent).  And that is the tip of the iceberg.

Vitamin B12 is involved with a staggering number of physiological functions including DNA, RNA, hormone, lipid and protein synthesis. Deplete vitamin B12 and a whole host of problems emerge, mostly neurological.

Vitamin B12 is critical for is the synthesis of the myelin sheaths around nerve fibers. There is a growing relationship between multiple sclerosis, which involves the disintegration of myelin and brain white matter and vitamin B12 deficiency.  Often the first signs of B12 deficiency are nervous system related with cognitive disturbances and peripheral neuropathy among the most common.

Additionally, many women have dysregulated hormones connected to vitamin B12 deficiency. In light of the Metformin mediated vitamin B12 deficiency, one has to wonder if some of the chronic health issues plaguing modern culture are not simply iatrogenic or medication induced.

Metformin, Pregnancy and Maternal and Fetal Complications

Considering that half the population is female, many of whom are on Metformin and may become pregnant, we must consider the potential effects of Metformin-induced vitamin B12 deficiency during pregnancy. As troubling as the effects are of B12 deficiency are on non-pregnant individuals, during pregnancy they can be devastating. Vitamin B12 deficiency during pregnancy leads to an increased incidence of neural tube defects and anencephaly (the neural tube fails to close during gestation). Once thought to be solely related to folate deficiency (vitamin B9) which Metformin also induces, researchers are now finding that B12 has a role in neural tube defects as well.

Scan the internet for Metformin and infertility and you’ll see long lists of fertility centers boasting the benefits of this drug. During pregnancy, the exuberance for vitamin M is palpable, although entirely misplaced. Early reports suggested Metformin would reduce an array of pregnancy complications including gestational diabetes. The data supporting these practices were mixed at best. At worst, however, they were downright incorrect. Metformin, it appears, may evoke the very conditions it was promoted to prevent during pregnancy and then some. Additionally, recent research suggests Metformin alters fetal development and induces long term metabolic changes in the offspring, likely predisposing the children to Type 2 Diabetes, an epigenetic effect perhaps.

Metformin Inhibits Exercise-Induced Insulin Sensitivity

As if those side effects were not enough to question mass Metformin prescribing practices, it appears that Metformin reduces any gains in insulin sensitivity that normally would be achieved from exercise. I cannot help but wonder if Metformin impairs insulin signaling in general. The cancer research suggests that it might.

According to one study, physical exercise can increase insulin sensitivity by up to 54% in insulin resistant individuals, unless of course, they are taking Metformin. Metformin abolishes any increased insulin sensitivity gained by exercise. Metformin also reduces peak aerobic capacity, reducing performance and making exercise more difficult. Moreover, despite claims to the contrary, Metformin does not appear to be an especially effective tool for weight loss, netting a reduction of only 5-10 pounds over 4-8 months. Regular exercise and a healthy diet net on average a loss of 5-10 pounds per month for most people and are significantly more effective at reducing diabetes and associated health complications without the potential side effects.

Metformin and Mitochondrial Damage

Perhaps most troubling amongst the Metformin side effects is its ability to severely impair mitochondrial functioning.

Recall from high school biology, the mitochondria are those bean shaped organelles inside cells that are responsible for cellular respiration or energy production. Through a variety of pathways, the mitochondria provide fuel for cell survival. In addition to cellular energy production, mitochondria control cell apoptosis (death), calcium, copper and iron homeostasis and steroidogenesis. In essence, mitochondria perform the key tasks associated with cell survival, and indeed, human survival. Damage the mitochondria and the cellular dysfunction or death will occur. Damage sufficient numbers of mitochondrion and chronic, multi-symptom illness arises.

As we have come to learn, many pharmaceuticals, environmental toxicants and even dietary deficiencies can impair mitochondrial functioning and induce disease processes that are often difficult to diagnose and treat. Metformin is no different. Metformin impairs mitochondrial functioning quite significantly by several mechanisms and, in doing so, sets off a cascading sequence of ill-effects.

At the center of metformin’s mitochondrial damage is its affect on the most basic of mitochondrial functions – ATP (cellular energy) production. Metformin reduces mitochondrial ATP production in skeletal muscle by as much as 48%. Sit with that one for a moment, a 48% reduction in cell fuel. Imagine functioning at only half capacity. This would make basic activities difficult at best and exercising to lose weight a very unlikely proposition. Imagine similar reductions in ATP production were observed in the brain or the heart or the GI tract (which, when on Metformin are likely), the types of disturbances we might see become quite clear: neurocognitive decline, psychiatric instability, neuropathy, heart rate, rhythm and blood pressure abnormalities, along with gastrointestinal distress to name but a few. Underlying all of these symptoms, and indeed, all mitochondrial dysfunction, is an overwhelming sense of fatigue and malaise.

Metformin Alters Immune Reactivity via the Mitochondria

As I wrote in a previous post:

Some researchers argue that the mitochondria are the danger sensors for host organisms; having evolved over two billion years to identify and communicate signs of danger to the cells within which they reside. The signaling is simple and yet highly refined, involving a series of switches that control cellular energy, and thus, cellular life or death. When danger is present, energy resources are conserved and the immune system fighters are unleashed. When danger is resolved, normal functioning can resume.

If the danger is not resolved and the immune battles must rage on, the mitochondria begin the complicated process of reallocating resources until the battle is won or the decision is made to institute what can only be described as suicide – cell death. Cell death is a normal occurrence in the cell cycle of life. Cells are born and die for all manner of reasons. But when cell death occurs from mitochondrial injury, it is messy, and evokes even broader immune responses, setting a cascade in motion that is difficult to arrest.

Metformin alters this process, first by damaging the mitochondrial ATP factory and reducing energy production capacity and then by inhibiting the signaling cascades that would normally respond to the danger signals. The double hit fundamentally alters immune function and I would suspect predisposes those who take Metformin to more infections and an array of inflammation based disease processes. More details on this in a subsequent post.

Metformin and the Statins: Beware

The mechanisms through which Metformin derails mitochondrial functioning are complex but likely related to depletion of coQ10, an enzyme involved in what is called the electron transport chain within the mitochondria. CoQ10, also referred to as ubiquinole and ubiquinone, is critical for mitochondrial functioning. Recall from a previous post, statins, like Lipitor, Crestor and others also deplete coQ10 and from a pharmacological perspective these mechanisms are implicated in the development of atherosclerosis and heart failure.

“statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and ‘heme A’, and thereby ATP generation.”

CoQ10 depletion is also implicated in the more common statin-induced side effects like muscle pain and weakness and in severe cases, rhabdomyolysis. Since Metformin and statins are regularly co-prescribed, the potential for severely depleted mitochondria and significant side effects is very high. Consider muscle pain and weakness among the first signs of problems.

My Two Cents

When we contrast the reduction in glucose mediated by Metformin with the damage this medication does to the mitochondria and immune signaling, along with its ability to leach vitamin B12, block insulin sensitivity and reduce aerobic capacity, one cannot help but wonder if we are causing more harm than good. Admittedly, obesity and hyperglycemia are growing problems in Western cultures. As we are coming to learn, however, obesity itself is not linked to the diseases processes for which many drugs like the statins and Metformin are promoted to protect against – obesity paradox. Growing evidence suggests that obesity is indicative of mitochondrial dysfunction and chemical exposures which then may provoke impaired insulin sensitivity and hyperglycemia and continued fat storage versus metabolism. If this is true, simply reducing circulating glucose concentrations, in an effort to reduce obesity and the purported health problems associated obesity, will do nothing to treat the underlying problem.

Insulin resistance and the associated hyperglycemia are environmental and lifestyle mediated problems that should be reversible with environmental and lifestyle changes. Having said that, those lifestyle and dietary changes will fail unless we consider the underlying mitochondrial damage initiated by dietary choices, pharmaceutical and other environmental exposures. For that we must dig deeper into mitochondrial functioning and correct what we can.

I believe obesity and hyperglycemia are symptoms of damaged and dysfunctional mitochondria, partly mediated by lifestyle, partly iatrogenic (pharmaceutically induced) and likely epigenetic. If we are to solve the ‘obesity’ problem and prevent the damage mediated by hyperglycemia, we have to address these variables. Failing to do so serves no one except those who profit from our continued ill-health.

Inline image 1
Robert Lamberton Consulting
Product Formulator of Professional Nutraceutical Products

Functional Medicine / Biological Age Reversal Consultant

Nutritional Therapy Practitioner (NTP)

Certified Light/Darkfield Microscopy Nutritionist

Author of the Biotics Research Educational Newsletter for Doctors

Contributing Writer / Advisory Board Member:

Nutricula: The Science of Longevity Journal 

Healthy Organic Woman Magazine

Twitter: rob_lamberton   Skype: larch60 Facebook: rlamberton  

LinkedIn ID


Phone: 778-227-4952

Taking Calcium Supplements Can Cause Brain Lesions

Taking calcium supplements — even at low doses — linked to brain lesions in the first study of its kind.

For the last several years, there has been ongoing controversy as to whether calcium supplementation is beneficial or harmful: probably the two areas where this gets the most focus would be related to osteopaenia/osteoporosis as well as the cardiovascular system.

Continue reading

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