Folic Acid Tied to a 44% Reduction in Suicide Attempts

 

Folic Acid Tied to a 44% Reduction in Suicide Attempts

Folic acid/vitamin B9, may provide a safe and effective approach for decreasing suicidal ideation, new research suggests. After adjusting for multiple factors, results from a large pharmaco-epidemiological study showed taking folic acid was associated with a 44% reduction in suicide events.

"These results are really putting folic acid squarely on the map as a potential for large-scale, population-level prevention," lead author Robert D. Gibbons, PhD, professor of biostatistics, Center for Health Statistics, University of Chicago, Illinois, told Medscape Medical News.

"Folic acid is safe, inexpensive, and generally available, and if future randomized controlled trials show this association is beyond a shadow of a doubt causal, we have a new tool in the arsenal," Gibbons said.

Having such a tool would be extremely important given that suicide is such a significant public health crisis worldwide, he added.

The findings were published online September 28, 2022 in JAMA Psychiatry.

Previous Research "Fairly Thin"

Folate, the naturally occurring form of B9, is essential for neurogenesis, nucleotide synthesis, and methylation of homocysteine. Past research has suggested that taking folate can prevent neural tube and heart defects in the fetus during pregnancy — and may prevent strokes and reduce age-related hearing loss in adults.

In psychiatry, the role of folate has been recognized for more than a decade. It may enhance the effects of antidepressants; and folate deficiency can predict poorer response to selective serotonin reuptake inhibitors (SSRIs).

This has led to recommendations for folate augmentation in patients with low or normal levels at the start of depression treatment.

Although previous research has shown a link between folic acid and suicidality, the findings have been "fairly thin," with studies being "generally small, and many are case series," Gibbons said.

The current study follows an earlier analysis that used a novel statistical methodology for generating drug safety signals that was developed by Gibbons and colleagues. That study compared rates of suicide attempts before and after initiation of 922 drugs with at least 3000 prescriptions.

Its results showed 10 drugs were associated with increased risk of suicide attempts after exposure, with the strongest associations for alprazolam, butalbital, hydrocodone, and combination codeine/promethazine. In addition, 44 drugs were associated with decreased risk, many of which were antidepressants and antipsychotics.

"One of the most interesting findings in terms of the decreased risk was for folic acid," said Gibbons.

He and his colleagues initially thought this was because of women taking folic acid during pregnancy. But when restricting the analysis to men, they found the same effect. Their next step was to carry out the current large-scale pharmaco-epidemiological study.

Prescriptions for Pain

Researchers used a health claims database that included 164 million enrollees. The study cohort was comprised of 866,586 adults with private health insurance (81.3% women; 10.4% aged 60 years and older) who filled a folic acid prescription between 2012 and 2017.

More than half of the folic acid prescriptions were associated with pain disorders. About 48% were for a single agent at a dosage of 1 mg/d, which is the upper tolerable limit for adults — including in pregnancy and lactation.

Other single-agent daily dosages ranging from 0.4 mg to 5 mg accounted for 0.11% of prescriptions. The remainder were multivitamins.

The participants were followed for 24 months. The within-person analysis compared suicide attempts or self-harm events resulting in an outpatient visit or inpatient admission during periods of folic acid treatment vs during periods without treatment.

During the study period, the overall suicidal event rate was 133 per 100,000 population, which is one fourth the national rate reported by the National Institutes of Health of 600 per 100,000.

After adjusting for age, sex, diagnoses related to suicidal behavior and folic acid deficiency, history of folate-reducing medications, and history of suicidal events, the estimated hazard ratio (HR) for suicide events when taking folic acid was 0.56 (95% CI, 0.48 to 0.65) — which indicates a 44% reduction in suicide events.

"This is a very large decrease and is extremely significant and exciting," Gibbons said.

He noted the decrease in suicidal events may have been even greater considering the study captured only prescription folic acid, and participants may also have also taken over-the-counter products.

"The 44% reduction in suicide attempts may actually be an underestimate," said Gibbons.

Age and sex did not moderate the association between folic acid and suicide attempts, and a similar association was found in women of childbearing age.

Provocative Results?

The investigators also assessed a negative control group of 236,610 individuals using cyanocobalamin during the study period. Cyanocobalamin is a form of vitamin B12 that is essential for metabolism, blood cell synthesis, and the nervous system. It does not contain folic acid and is commonly used to treat anemia.

Results showed no association between cyanocobalamin and suicidal events in the adjusted analysis (HR, 1.01; 95% CI, 0.80 - 1.27) or unadjusted analysis (HR, 1.02; 95% CI, 0.80 - 1.28).

Gibbons noted this result boosts the argument that the association between folic acid and reduced suicidal attempts "isn't just about health-seeking behavior like taking vitamin supplements.”

Another sensitivity analysis showed every additional month of treatment was associated with a 5% reduction in the suicidal event rate.

"This means the longer you take folic acid, the greater the benefit, which is what you would expect to see if there was a real association between a treatment and an outcome," said Gibbons.

The new results "are so provocative that they really mandate the need for a well-controlled randomized controlled trial of folic acid and suicide events," possibly in a high-risk population such as veterans, he noted.

Such a study could use longitudinal assessments of suicidal events, such as the validated Computerized Adaptive Test Suicide Scale (CAT-SS), he added. This continuous scale of suicidality ranges from sub-clinical, signifying helplessness, hopelessness, and loss of pleasure, to suicide attempts and completion.

As for study limitations, the investigators note that this study was observational, so there could be selection effects. And using claims data likely underrepresented the number of suicidal events because of incomplete reporting. As the researchers point out, the rate of suicidal events in this study was much lower than the national rate.

Other limitations cited were that the association between folic acid and suicidal events may be explained by healthy user bias; and although the investigators conducted a sensitivity analysis in women of childbearing age, they did not have data on women actively planning for a pregnancy.

"Impressive, Encouraging"

Commenting for Medscape Medical News, Shirley Yen, PhD, associate professor of psychology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, described the new findings as "quite impressive" and "extremely encouraging.”

However, she noted "it's too premature" to suggest widespread use of folic acid in patients with depressive symptoms. Yen, who has researched suicide risks previously, was not involved with the current study.

She did agree with the investigators that the results call for "more robustly controlled studies. These could include double-blind randomized controlled trials that could "more formally assess" all folic acid usage as opposed to prescriptions only, Yen said.

The study was funded by the National Institutes of Health, the Agency for Healthcare Research and Quality, and the Center of Excellence for Suicide Prevention (US Department of Veterans Affairs). Gibbons reported serving as an expert witness in cases for the US Department of Justice; receiving expert witness fees from Merck, GlaxoSmithKline, Pfizer, and Wyeth; and having founded Adaptive Testing Technologies, which distributes the Computerized Adaptive Test Suicide Scale. Yen has reported no relevant financial relationships.

Reference: JAMA Psychiatry. Published online September 28, 2022. doi:10.1001/jamapsychiatry.2022.2990. Association Between Folic Acid Prescription Fills and Suicide Attempts and Intentional Self-harm Among Privately Insured US Adults <https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2796907?guestAccessKey=9b279b0a-926b-4561-8b55-e943fd904f8e&utm_source=silverchair&utm_medium=email&utm_campaign=article_alert-jamapsychiatry&utm_content=olf&utm_term=092822>

Are you returning the favor?

 This was interesting for me to ponder recently. I was experiencing some emotional upheaval and dis-regulation. We sometimes go through these clearing phases where everything feels overwhelming and I could have cried at the drop of a hat.

I am always there for any friends or family that need a shoulder to cry on or needs to vent or just have someone to listen without judgement or need to fix anything. (women will understand this) and it occurred to me that I am not as readily open to allowing those friends to return the favor. I tend to seclude myself when I am going through some emotional struggles and I do not always reach out for that shoulder or loving ear.

That is why I ask, are you open to returning the favor.

Our friends and family wish to be there for us too. They will lovingly listen and offer kind words and friends will be ready with some hard hitting wisdom.

It made me think about what this resistance to open up says about me...why do I behave this way?

Could it be that I have some underlying beliefs around self worth? Do I not feel deserving? Is it fear of being vulnerable or do I not believe that anyone has earned the right to hear my deepest darkest fears, thoughts and challenges?

And if I think the last statement is true then why have I not cultivated such a tribe?

I am grateful for the friends that I can turn to (you know who you are) and for their wisdom and for never being afraid to tell me the truth even when it is uncomfortable to hear and to offer a change in perspective whenever I need it.

Thinking about all of this and looking deeper within has also helped me get out of my funk and given me new motivation to create the life and community I desire and to create more health, happiness and joy, not just for myself, for all whom I associate and commune with. It has also made me look at how i treat myself and ask the question, am I a friend to myself? am I gentle and nurturing to myself?

Am I returning the favor....I may not have been as open to doing so in the past and with greater awareness of this, I am choosing to be open to returning the favor when needed. I am open to receive.

 

The One Emotion that Extends Your Life

Ronald Grisanti D.C., D.A.B.C.O., DACBN, MS, CFMP

Based on progressive research we find that what we think about and what we feel have far-ranging effects on our immune system.

One important part of our immune system includes the natural killer cell or NK cells. These are a type of lymphocyte and an important player in the war on invading bad microbes and mounting an immune attack to combat these bad microbes. NK cells are known to be protective against cancer. Some studies have documented that the less active your NK cells are the more rapid cancer progression and the more it spreads throughout the body.

And guess what?

These important NK cells actually respond to your mood.

The most important emotion to boost these NK cells is laughter.

When you are feeling good, optimistic and happy your NK cells multiply exponentially!

If you are known pessimist, there is still hope for you.

A study done at the University of California showed that actors who spent time performing depressing movie scenes had a decreased immune responsiveness. On the other hand actors who performed roles where they were uplifting, had an increased immune responsiveness. So the moral of the story is something called, Fake it till you make it. Yes, even if you don't feel happy, at least act like you do! Your body's immune system will reward you for it.

Here is a good punch list to improve your mood and of course boost your NK cells: These include: watching funny movies, making music or listening to uplifting music, coloring in books, walking in the woods, going to a comedy show, spending time with good uplifting friends to something as simple as taking a soaking bath with relaxing herbs.

(Functional Medicine University)

References:

https://pubmed.ncbi.nlm.nih.gov/12652882

https://pubmed.ncbi.nlm.nih.gov/11712080

https://www.sciencedaily.com/releases/2010/04/100426113058.htm

The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of Dr. Grisanti and his functional medicine community. Dr. Grisanti encourages you to make your own health care decisions based upon your research and in partnership with a qualified health care professional.

Antiviral Lactoferrin Now pitted against COVID-19

Antiviral Lactoferrin Now Pitted Against COVID-19

 by Noelle Patno, PhD

Lactoferrin (LF) has been advocated by researchers1–3 as a potential method to prevent or treat COVID-19. These recent reviews promote a hypothesis that the natural, endogenous compound which has shown antiviral capabilities for other viruses including SARS-CoV may be effective against the SARS-CoV-2 virus as well. With over 70 years since the discovery of this glycoprotein, this iron-scavenging milk protein now deserves greater attention. The current literature demonstrates that LF has many anti-inflammatory, immunomodulatory, and even anticarcinogenic effects; what remains to be discovered is its specific activity against the pandemic virus of our times, SARS-CoV-2. A large body of in vitroevidence suggests that lactoferrin may have efficacy because of its ability to inhibit viruses and bind to viral surface receptors, which are related to SARS-CoV-2 mechanisms. Now is the time to discover more about this glycoprotein and its potential against SARS-CoV-2.

Mechanism of binding to heparan sulfate

A recent paper (published in Cell, November 2020) demonstrated that SARS-CoV-2 infection depends on attachment to cellular heparan sulfate (HS) and ACE2.4 While ACE2’s role was predicted in January5 and subsequently demonstrated in March,6 this revelation in November reveals the importance of HS as an essential factor in the virus’s attachment and entry to infect the cell. Heparan sulfate, a complex carbohydrate on almost every cell’s surface, is useful to the host to determine the cell’s response to stimuli such as metabolic or inflammatory stimuli and critically as part of immune functions.7 However, many viruses hijack HS to bind and depend on it for their infection. In vitro evidence supports this mechanism for other viruses including the Nipah and Hendra viruses;8 entrovirus 71, which is associated with hand foot mouth disease;9 enteroaggregative E. coli, which is a significant cause of diarrhea and foodborne outbreaks;10 rift valley fever virus;11 and human papillomavirus.12 This list overlaps with the list of pathogenic viruses that lactoferrin inhibits in vitro, which includes but is not limited to the following: herpes simplex virus, hepatitis B virus, hepatitis C virus (HCV), avian flu, enterovirus 71, Japanese encephalitis virus, respiratory syncytial virus, influenza A virus, parainfluenza virus, cytomegalovirus, poliovirus, rotavirus, and human immunodeficiency virus (HIV), with clinical evidence for enterovirus 71, HCV, norovirus, and rotavirus.2 With lactoferrin’s previous ability demonstrated to prevent the Japanese encephalitis virus,13 alphavirus,14 Toscana virus,15 dengue virus,16 and the SARS pseudovirus17 from entering cells through HS receptors and infecting the cells, then LF has the possibility of preventing SARS-CoV2 from entering cells as well.

Potential mechanisms by which LF might help against SARS-CoV-2 are therefore the following:1

Prevent attachment to heparan sulfate receptors on the cell and inhibit viral entry4,13
Prevent attachment to ACE2 and inhibit viral entry/infection of the cell18

Prevent attachment to DC-SIGN, dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin receptor and thereby prevent infection of the cell3
Prevent attachment and viral entry via other receptors17

Inhibit viral replication15,19
Decrease IL-6,20 which is part of the cytokine storm

Current clinical trials evaluating lactoferrin in COVID-19

The table below lists the current clinical trials on clinicaltrials.gov evaluating lactoferrin in COVID-19.

Three recent publications further suggest that lactoferrin may help against SARS-CoV-2:

1. In vitro, bovine lactoferrin was able to decrease significantly the numbers of SARS-CoV-2-infected bronchial epithelial cell mimetics, the single compound mentioned in the abstract of the preprinted paper, and one of 17 dose-responsive compounds from a 1,425 library in a drug-repurposing high throughput screen19

2. The completed randomized clinical study listed above, in 32 patients with confirmed COVID-19 by RT-PCR, showed an early clearance of the virus, recovery from symptoms, and statistically significant reduction in IL-6 , with additional in vitro and in silico support for lactoferrin’s ability to prevent cells from infection through preincubation as well as simulated binding of lactoferrin to the ACE2 receptor.18

3. A 10-day study evaluating the effect of a liposomal bovine lactoferrin syrup that included vitamin C alone or with zinc (for a total of 256 to 384 mg of lactoferrin per day) and additional nasal and mouth spray or aerosol application for additional symptoms. IgM/IgG antibody rapid test in whole blood was used for confirmed COVID-19 diagnosis in 75 people. Symptoms were scored on a scale of 0 to 3 in severity twice a day for 10 days and then a follow-up after one month. By the fifth day, all patients recovered from respiratory distress and headache symptoms. The percentage of patients without symptoms of coughing, muscular pain, nasal congestion, tiredness, and diarrhea all increased by 48 hours and 5 days after study start.21

There are many limitations to the above three studies. The first two preprinted articles have not been peer-reviewed. The third lacked clear dosing instructions, did not use the more accurate SARS-CoV-2 diagnostic tests; did not follow-up test for the virus after-treatment; used additional interventions for subsets of patients; lacked more rigorous, randomized, and controlled design and more objective and validated methodology; and was not the complete data set for the study, among other limitations. Clinical studies on the effects of lactoferrin supplementation in COVID-19 patients is a promising and interesting research advancement to watch.

Citations

1. Campione E et al. Lactoferrin as protective natural barrier of respiratory and intestinal mucosa against coronavirus infection and inflammation. Int J Mol Sci. 2020;21(14):4903.

2. Chang R et al. Lactoferrin as potential preventative and adjunct treatment for COVID-19. Int J Antimicrob Agents. 2020;56(3):106118.

3. Wang Y et al. Lactoferrin for the treatment of COVID-19 (Review). Exp Ther Med. 2020;20(6).

4. Clausen TM et al. SARS-CoV-2 infection depends on cellular heparan sulfate and ACE2. Cell. 2020;183(4):1043-1057.e15.

5. Wan Y et al. Receptor recognition by the novel coronavirus from Wuhan: an analysis based on decade-long structural studies of SARS coronavirus. J Virol. 2020;94(7).

6. Hoffmann M et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell. 2020;181(2):271-280.e8.

7. Simon Davis DA et al. Heparan sulfate: a ubiquitous glycosaminoglycan with multiple roles in immunity. Front Immunol. 2013;4.

8. Mathieu C et al. Heparan sulfate-dependent enhancement of henipavirus infection. mBio. 2015;6(2).

9. Kobayashi K et al. Heparan sulfate attachment receptor is a major selection factor for attenuated enterovirus 71 mutants during cell culture adaptation. PLOS Pathogens. 2020;16(3):e1008428.

10. Rajan A et al. Enteroaggregative E. coli adherence to human heparan sulfate proteoglycans drives segment and host specific tesponses to infection. PLOS Pathogens. 2020;16(9):e1008851.

11. de Boer SM et al. Heparan sulfate facilitates Rift Valley fever virus entry into the cell. J Virol. 2012;86(24):13767-13771.

12. Selinka H-C et al. Inhibition of transfer to secondary receptors by heparan sulfate-binding drug or antibody induces noninfectious uptake of human papillomavirus. J Virol. 2007;81(20):10970-10980.

13. Chien Y-J et al. Bovine lactoferrin inhibits Japanese encephalitis virus by binding to heparan sulfate and receptor for low density lipoprotein. Virology. 2008;379(1):143-151.

14. Waarts B-L et al. Antiviral activity of human lactoferrin: inhibition of alphavirus interaction with heparan sulfate. Virology. 2005;333(2):284-292.

15. Pietrantoni A et al. Bovine lactoferrin inhibits Toscana virus infection by binding to heparan sulphate. Viruses. 2015;7(2):480-495.

16. Chen J-M et al. Bovine lactoferrin inhibits dengue virus infectivity by interacting with heparan sulfate, low-density lipoprotein receptor, and DC-SIGN. Int J Mol Sci. 2017;18(9).

17. Lang J et al. Inhibition of SARS pseudovirus cell entry by lactoferrin binding to heparan sulfate proteoglycans. PLoS One. 2011;6(8). doi:10.1371/journal.pone.0023710

18. Campione E et al. Pleiotropic effect of Lactoferrin in the prevention and treatment of COVID-19 infection: randomized clinical trial, in vitro and in silico preliminary evidences. bioRxiv. Published online August 17, 2020:2020.08.11.244996.

19. Mirabelli C et al. Morphological cell profiling of SARS-CoV-2 infection identifies drug repurposing candidates for COVID-19. bioRxiv. Published online September 28, 2020.

20. Lepanto MS et al. Efficacy of lactoferrin oral administration in the treatment of anemia and anemia of inflammation in pregnant and non-pregnant women: an interventional study. Front Immunol. 2018;9.

21. Serrano G et al. Liposomal lactoferrin as potential preventative and cure for COVID-19. Int J Res Health Sci. 2020;8(1):8.

Noelle Patno, PhD is the Nutrition Scientist for Digestive Health at Metagenics. Dr. Patno received her PhD in Molecular Metabolism and Nutrition and Masters in Translational Science from the University of Chicago, studying the role of microbial components in intestinal epithelial cell survival related to inflammatory bowel disease. Prior to her graduate studies, Dr. Patno received a chemical engineering degree from Stanford University and worked as an engineer. She has personal experience and interest in preventive nutrition and nutritional therapies for chronic disease, and her current role involves researching and developing probiotics, prebiotics, and other nutritional programs for the promotion of digestive and overall health.

 

Are Artificial Sweeteners Really Harmless?

Medscape Medical News - August 19, 2022

New research discounts the long-held notion that aspartame and other nonnutritive sweeteners (NNS) have no effect on the human body.

In a study, researchers found that these sugar substitutes are not metabolically inert and can alter the gut microbiome in a way that can influence blood glucose levels.

The study was published online August 19,20-22 in the journal Cell.

Gut Reaction? 

Several years ago, a team led by Eran Elinav, MD, PhD, an immunologist and microbiome researcher at the Weizmann Institute of Science, Rehovot, Israel, observed that NNS affect the microbiome of mice in ways that could affect glycemic responses.

They have now confirmed this observation in a randomized controlled trial with 120 healthy adults.

Before the study, all participants strictly avoided NNS. During the trial, some remained NNS-free, while others used saccharin, sucralose, aspartame, or stevia daily for 2 weeks in doses lower than the acceptable daily intake.

Each NNS "significantly and distinctly" altered stool and oral microbiome, and two of the sweeteners (saccharin and sucralose) significantly impaired glucose tolerance, the researchers report.

"Importantly, by performing extensive fecal transplantation of human microbiomes into germ-free mice, we demonstrate a causal and individualized link between NNS-altered microbiomes and glucose intolerance developing in non-NNS-consuming recipient mice," they say.

They note that the effects of these sweeteners will likely vary from person to person because of the unique composition of an individual's microbiome.

"We need to raise awareness of the fact that NNS are not inert to the human body as we originally believed. With that said, the clinical health implications of the changes they may elicit in humans remain unknown and merit future long-term studies," Elinav said in a news release.

For now, Elinav says it's his personal view that "drinking only water seems to be the best solution.”

Weighing the Evidence 

Several experts weighed in on the results in a statement from the UK nonprofit organization, Science Media Centre.

Duane Mellor, PhD, RD, RNutr, registered dietitian and senior teaching fellow, Aston University, Birmingham, United Kingdom, notes that the study does not show a link between all NNS and higher blood glucose levels in the long term (only after a glucose tolerance test).

"It did suggest, though, that some individuals who do not normally consume sweeteners may not tolerate glucose as well after consuming six sachets of either saccharin or sucralose mixed with glucose per day," Mellor says.

Kim Barrett, PhD, distinguished professor of physiology and membrane biology, University of California, Davis, School of Medicine, concurs, saying, "this well-designed study indicates the potential for NNS to have adverse effects in at least some individuals."

The study also does not provide any information about how people who normally consume sweeteners or people with either type 1 or type 2 diabetes respond to NNS.

"Therefore, for some people, it is likely to be a better option and more sustainable approach to use sweeteners as a 'stepping stone,' allowing them to reduce the amount of added sugar in foods and drinks, to reduce their sugar intake, and still enjoy what they eat and drink, on the way to reducing both added sugar and sweeteners in their diet," Mellor suggests.

Kevin McConway, PhD, with the Open University, Milton Keynes, United Kingdom, says it's "important to understand that the research is not saying that these sweeteners are worse for us, in heath terms, than sugar.

"But exactly what the health consequences of all this, if any, might be is a subject for future research," McConway adds.

Kathy Redfern, PhD, lecturer in human nutrition, University of Plymouth, UK, agrees.

"We still have a lot to learn about the human microbiome, and although this study suggests two of the sweeteners tested in this study (sucralose and saccharin) significantly affected glucose tolerance, these deviations were small," she says.

The International Sweeteners Association also weighs in, saying, "No conclusions about the effects of low/no calorie sweeteners on glucose control or overall health can be extrapolated from this study for the general population or for people who typically consume sweeteners, including people living with diabetes."

They add that "a recent review of the literature concluded that there is clear evidence that changes in the diet unrelated to low/no calorie sweeteners consumption are likely the major determinants of change in gut microbiota."

Nevertheless, Redfern says the results "warrant further investigation to assess how small changes in glucose tolerance in response to NNS consumption may influence longer term glucose tolerance and risk for metabolic complications, such as type 2 diabetes."

The study had no specific funding. Elinav is a scientific founder of DayTwo and BiomX, a paid consultant to Hello Inside and Aposense, and a member of the scientific advisory board of Cell. Mellor has provided consultancy to the International Sweetener Agency and has worked on projects funded by the Food Standards Agency that investigated the health effects of aspartame. Barrett, McConway, and Redfern report no relevant financial relationships. 

Cell. Published online August 19, 2022. <https://www.cell.com/cell/fulltext/S0092-8674(22)00919-9>

Living on purpose

 During my meditation and movement practice this morning, I contemplated the meaning and expanse of living on purpose, or I could say the thought hit me like a freight train.

As can only happen in these energetic spaces, I was flooded with the concept:

ON PURPOSE...Intentionally, my reason for being and doing.

Purpose...the reason for which something is done or created or for which something exists. (noun)...Verb: Have as one's intention or objective.

So many of us struggle to find our purpose and I can honestly say that I am not sure if I have or haven't,  however I do believe it has something to do with what we chose to focus on, our intent, and we get to chose on a daily basis. It is therefore a good practice for me to mediate and move every morning to chose and be clear on what my focus or intent for the day will be.

I have chosen to focus on more love, and to live on purpose (intentionally). Meaning I have chosen to live my life with the purpose of opening up to more love for myself and to spread and share more love with others and through my work, I intend to help open the hearts of humanity to the love of the soul. I am choosing to see the miracle in everyone and everything.

Is that my purpose??? 

All I can do is to wake up every day and live on purpose and chose to do so all day. And for now that purpose is love, and I believe that with this intent and focus, I will be more fulfilled and it will lead to a deeper how and an even deeper purpose and my purpose will continue to unfold in more miraculous ways.

 

Are Diabetics Being Cheated?

Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., M.S., CFMP

A recent patient was concerned that despite watching her diet and taking her diabetes medication her hemoglobin A1C (HbA1c) keeps going up.

Remember, HbA1c is a lab test that shows the average level of blood sugar (glucose) over the previous 3 months. It shows how well you are controlling your diabetes. 

An elevated HbA1c greater than 5.7% indicates that the diabetes is not well regulated and is in fact accelerating aging, increasing your chances of getting painful neuropathies, kidney failure needing dialysis, cataracts, amputations, and retinopathy blindness.

What could possibly be missed by her primary doctor?

One major cause of the unregulated glycosylated hemoglobin is an unrecognized B6 deficiency.

An excellent “functional” test to check for a pyridoxine (B-6) deficiency is the xanthurenate organic acid test. An elevated xanthurenate test is a sensitive marker for a B-6 deficiency.

 

This is an Organic Acid Test from Genova

But wait.. there is more to the story.

You can take B-6 and it may not work.

Why?

Because of a zinc deficiency.

When hidden zinc deficiency is present, the body cannot convert B6 to its active form, pyridoxal-5-phosphate or P5P. P5P, essential in normalizing the glycosylated hemoglobin and its deficiency, is an indicator that improperly metabolized sugars are accelerating aging, cataracts, kidney failure, heart disease, nerve damage and more.

This is the intracellular nutrient test from Doctor's Data

But there is more to the story.

Elevated stored phthalates (plastics) in the body interfere with zinc metabolism.

This is a Phthalate Test from Genova

This is the power of functional medicine. Seeking to find the cause of the cause of the cause.

HbA1c ---> B-6 deficiency ---> Zinc deficiency ---> Stored Phthalates

I have never yet met a diabetologist who even orders the above much less knows how to interpret it.

To ignore fixing the chemistry in an overtly metabolic disease is outright wrong.

Unfortunately, what I have seen from reading thousands of medical records is the fact that most doctors merely resort to the one size fits all approach and medicate the disease. Rarely if ever have I read where a doctor investigated why the HA1C was elevated.

This results in a tragic waste of life as well as incurring an enormous and unnecessary expense and suffering.

You may be interested to know that because of the phthalate load, many folks (even without diabetes) unnecessarily get multiple diseases. These can range from Nonalcoholic steatohepatitis or NASH (a common, often “silent” liver disease), heart disease or cancers to Parkinson's disease, arthritis, or Alzheimer's.

Clearly they all lead to accelerated aging because of the shared causes.

For a doctor to check your glycosylated hemoglobin A1C every 3 months yet never know your zinc and B6 levels (among many others) is plain wrong in this sophisticated era.

Your life depends on the decisions you make. This information has a huge bearing on whether your diabetes blinds you in future years.

 

References:

Depeint F, et al, Mitochondrial function and toxicity: Role of B vitamins, one-carbon transfer pathways, Chemico-Biological Interactions 163:113-32, 2006

Jain SK, et al, Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation and (Na+ + K+)-ATPase activity reduction in high glucose-treated human erythrocytes, Free Rad Biol Med 30:232-37, 2001

Onarato JM, et al, Pyridoxamine, an inhibitor of glycation reactions, also inhibits lipid peroxidation reactions, J Biol Chem, 275:21177-84, 2000

Metz TO, et al, Pyridoxamine traps intermediates in lipid peroxidation reactions in vivo: evidence on the role of lipids and chemical modification of protein and development of diabetic complications, J Biol Chem 278:42012-19, 2003

Booth AA, et al, Thiamine pyrophosphate and pyridoxamine inhibit the formation of antigenic advanced glycation endproducts: comparison with aminoguanidine, Biochem Biophys Res Commun, 220:113-19, 1996

Stitt A, et al, The AGE inhibitor pyridoxine and inhibits development of retinopathy in experimental diabetes, Diabetes 51:2826-32, 2000

Laines-Cessac P, et al, Mechanisms of the inhibition of human erythrocyte pyridoxal kinase by drugs, Biochem Pharmacol 54:863-70, 1997

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