Traumatic brain injury (TBI) is a leading cause of death and disability. It is also a debilitating and heavily stigmatized condition that all too often goes undiagnosed and untreated, leaving sufferers without hope of recovery. Current treatments are largely ineffective. Join Olympia based naturopathic physician Dr. Thomas Griffith for a discussion of his preferred treatment for TBI- intravenous DMSO, a compound made during the processing of tree pulp. Passionate about finding safe and effective treatments for serious conditions, Dr. Griffith will present evidence from clinical trials that DMSO is a promising therapy for sever traumatic brain injury.  

This is an image of Phinneas Gage, a famous TBI victim who actually lived to tell the tale.

Dr. Griffith recommends visiting DMSO.org before attending the presentation, to familiarize yourself with the history and research about DMSO.

Clinical human trials are confirming the strong performance of prunes in reversing osteoporosis in animal studies. The exact mechanism of action is still not clear but it has been noted that prunes are a rich source of selenium and boron, both necessary in bone metabolism and mineralization. The polyphenols in prunes are known to down regulate inflammatory and catabolic biochemical pathways (breakdown) resulting in less bone loss and more synthesis. Many other fruits contain similar polyphenols but prunes have proven to be the most effective fruit for preventing and reversing bone loss.

A recent study by Dr. Bahram Arjmandi of Florida State University was published in the Journal of Medicinal Plants May 2011. This study of 160 postmenopausal osteopenic (decreased bone density) women, “not on hormone replacement therapy or any other prescribed medication known to influence bone metabolism”, demonstrated the ability of prunes to not only prevent bone lose but to actually reverse bone loss and increase bone density with administration of just 100 grams of prunes per day (roughly 10 prunes). Given the significant potential for side effects from current standard of care prescriptive medications, this study calls to question the necessity of those drugs. It also infers that consumption of prunes before the onset of bone loss may be preventative of osteoporosis.

The mechanism behind prunes effects on bone density may not be fully elucidated, but from a Naturopathic perspective it is clear. Prunes provide fiber which enhance the bowels ability to eliminate toxins and byproducts of metabolism. Fiber provides food for beneficial gut bacteria which in turn provide cells of the colon with short chain fatty acids as a breakdown product of the fiber they digest. Short chain fatty acids are a food to colon cells and help them to function more optimally. The types of bacteria fed by the fiber from prunes are capable of modulating the immune system to a less reactive and less inflammatory response. Inflammation has been linked to increased bone degeneration.

The improvements in bowel function also lead to greater absorption of food which is especially important when it comes to bone supporting nutrients like Vitamin D, Calcium, Magnesium, selenium, boron and of course bone building polyphenols. From an ND’s perspective these mechanisms of prune action on bone density are obvious. This theory is further supported by the fact another study published in April 2010 by Dr. Arjmandi in the Journal of Medicinal Food showed that a combination of a type of fiber called fructo-oligosaccharides (FOS) and dried plum provided added benefit in restoring bone density in rats. The combination of FOS and plum was more effective than plum combined with additional polyphenols.

It’s amazing how much research it takes to pull the nectar of knowledge out of a deliciously simple prune and discover the potent benefits within. Thanks to Dr. Arjmandi and his team at FSU for bringing food back to the table as medicine. It is time we moved away from the notion that medicine must be equated to a pill. I sure hope the price of prunes doesn’t go up because of this…

Stay well,

Doc Griffith

I’ve posted three articles below that focus on infectious organisms detectable in the blood stream and their role in the onset and progression of coronary artery disease / atherosclerosis. The consequence of uncontrolled coronary artery disease is myocardial infarction or heart attack, one of the top killers in the US. Though there is still debate about the extent these infectious microbes contribute to atherosclerosis, the evidence suggests that the greater number of different organisms detectable the greater severity of progression towards arterial disease. There have also been studies confirming improved vascular function after use of anti-microbial agents like anti-biotics.

For years the primary focus of treatment of coronary artery disease treatment and research has focused on reducing LDL cholesterol with statin drugs. Now we are seeing evidence mounting that the cholesterol may just be merely kindling and that environmental factors such as infectious agents may be the match to light the fire. Genetics likely dictate how far, fast and furiously the fire burns. Statin drugs are the most prescribed and studied means of treating these risks. The research, funded by big Pharma, has been myopically focused on statins ability to lower LDL cholesterol, and they do apparently reduce risk. Some would argue the risk reduction is marginal and is not worth the common adverse effects of statins that have made them unpopular with many patients. What is left out of the discussion and research is the fact that statins are potent anti-inflammatories and their protection may be conferred by putting out the match. The role of infectious organisms is still not definitive as there is not nearly enough research done on therapies, other than LDL reduction by statins, to actually bring other causation to light.

What the evidence calls to question about infectious disease presence in these patients is whether there may be other ways of turning down the heat like addressing infectious agents and other causative factors. Conventionally the primary means of treating infection is with the use of anti-microbial drugs but these are rarely used for atherosclerosis outside of a research setting. Fortunately, as an Naturopathic physician, there are many tools to reduce the threshold of inflammatory and hyper-coagulative (sticky platelets and cholesterol) responses that create the susceptibility to developing atherosclerosis. A basic naturopathic approach may include: Exercise and lifestyle, anti-inflammatory dietary modification, anti-oxidants, natural antimicrobials, cholesterol lowering agents and blood thinners, gastrointestinal and immune support, cardio-protective and supportive herbs and nutrients, elimination of environmental toxins, as well as IV treatments such as intravenous vitamin C, lipoic acid, phosphatidylcholine and dmso (all show promise in reducing vascular damage of atherosclerosis). These approaches address the basic pathophysiology of atherosclerosis, not just the numbers on a cholesterol panel.

The research implicating other risk factors besides LDL cholesterol continues to mount and I foresee a future where the dominance of the LDL hypothesis for coronary artery disease is put into perspective. LDL cholesterol is not typically the cause atherosclerosis plaques it is a consequence of vessels that have taken a beating from high blood pressure, tissue damage, oxidation and inflammation. LDL cholesterol acts to reinforce the vascular wall to protect the coronary artery. It is the environment that dictates the susceptibility. Infectious disease presence is but one of many factors that should be taken into account to get the full picture. It is important that we expand our notions of causation with cardiovascular disease like atherosclerosis in order to do more than treat laboratory values but to actually reach closer and closer towards treating the cause and the whole patient. It is after all the whole patient that truly heals their own heart, not their practitioner or their pills.

Be well,

Doc Griffith

Nihon Rinsho. 2011 Jan;69(1):25-9.
[Etiology of atherosclerosis-- special reference to bacterial infection and viral infection].
[Article in Japanese]
Kurano M, Tsukamoto K.
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo.

Abstract

Atherosclerosis is caused by multiple factors. Infectious disease has been proposed to be one of the causative factors, and several bacteria and viruses have been studied for their correlations with atherosclerotic diseases; these organisms include Chlamydia pneumoniae, Helicobacter pylori, HIV, CMV, HSV and hepatitis viruses. Many underlying mechanisms that infectious diseases cause atherosclerosis have been proposed; most of them suggested that inflammatory process provoked by infectious diseases led to atherosclerosis. Several clinical studies were also performed to examine whether treatment for infectious diseases could protect against atherosclerosis. However, the relationship between infectious diseases and atherosclerotic diseases and the effects of treatment for infectious diseases on atherosclerosis are still controversial; there are both positive and negative reports. Thus, further studies are needed to clarify the correlation.

Journal of Clinical Virology
Volume 32, Issue 1, January 2005, Pages 29-32

Detection of herpes simplex virus, cytomegalovirus and Epstein-Barr virus DNA in atherosclerotic plaques and in unaffected bypass grafts

Ali I. Ibrahima, Michel T. Obeida, Muhidien J. Joumaa, Ghassan A. Moasisb, Wael L. Al-Richaneb, Ingrid Kindermannc, Michael Boehmc, Klaus Roemerd, Nikolaus Mueller-Lantzschd, Barbara C. Gärtnerd, Corresponding Author Contact Information, E-mail The Corresponding Author
Purchase
Department of Clinical Chemistry and Microbiology, University of Damascus, Syria
Department of Cardiovascular Surgery, Assad University Hospital, Damascus, Syria
Department of Cardiology, University of the Saarland, 66421 Homburg/Saar, Germany
Department of Virology, University of the Saarland, 66421 Homburg/Saar, Germany

revised 28 June 2004; Accepted 28 June 2004. Available online 23 August 2004.
Abstract

Background: Herpes virus infections are suspected to be involved in the pathogenesis of atherosclerosis. Objective and method: Viral DNA of herpes simplex virus (HSV), Epstein-Barr virus (EBV) and cytomegalovirus (CMV) was analyzed by real-time PCR on 48 biopsies from atherosclerotic plaques extracted by end-arterectomy (46 coronary arteries, 2 carotid arteries), and in tissue from non-atherosclerosis vessels from the same patient as controls (23 internal mammary arteries, 43 saphenous veins). Results: HSV-1 DNA was detected significantly more frequently in plaques (35%) than in control veins (9%, P = 0.006). However, the frequency of HSV-1 DNA detection in the internal mammary artery grafts was as high as in plaques (22%, P = 0.28). CMV and EBV DNA were exclusively found in plaques but not in controls, with 10% for CMV (P = 0.06 versus veins, P = 0.17 versus graft arteries) and 2% for EBV (P = 1.0), respectively. HSV-2 was neither detected in plaques nor in controls. Herpes viral DNA was significantly associated only with arterial hypertension but not with other classical risk factors (P = 0.02), in accordance with the hypothesis that herpes viral infection may alter the vessel wall. Conclusion: We conclude that herpes viral infections may have a role in atherosclerosis and that the presence of herpes viral DNA in the grafts used for bypass surgery might constitute a potential risk for atherosclerosis or restenosis.

Abbreviations: PCR, polymerase chain reaction; HSV, herpes simplex virus; CMV, cytomegalovirus; EBV, Epstein-Barr virus; CAD, coronay artery disease; vs., versus

Editorials – Circulation Research. 2008; 102: 861-863

Chlamydophila pneumoniae and Endothelial Activation
The Smoke That Precedes the Fire of Atherosclerosis?
Sean P. Didion
From the Department of Internal Medicine, Division of Cardiovascular Medicine, The University of Iowa Carver College of Medicine, Iowa City.

Correspondence to Sean P. Didion, PhD, Department of Internal Medicine, Division of Cardiovascular Medicine, The University of Iowa Carver College of Medicine, 340-G Eckstein Medical Research Building, Iowa City, IA 52242. E-mail sean-didion@uiowa.edu

Exactly 100 years ago, the physician Sir William Osler suggested an important role for inflammation, as well as infection, in the pathogenesis of atherosclerosis.1 Indeed, it is now well accepted that atherosclerosis is a disease with a large inflammatory component.2 In addition to traditional risk factors, such as hypertension, hyperlipidemia, diabetes, and smoking, previous, as well as chronic or recurrent, infection has emerged as a novel risk factor for atherosclerosis. Cytomegalovirus, herpes simplex virus, Helicobacter pylori, and hepatitis A are a few examples of pathogenic agents that have been, in 1 form or another, associated with atherosclerosis.3 However, no association appears to have garnered more attention, or plausibility, than that between Chlamydophila pneumoniae (formerly Chlamydia pneumonia) infection and atherosclerosis.

To those of us who have been labelled as quacks, charlattans or fear mongers for suggesting just such a thing, research like this is validation by way of hard science. The truth is that low levels of environmental pollutants are found in all of us and they do promote disease. This has been known in the case of developing infants and children for a long time but still hasn’t led to prioritization of research, govermental or medical practices towards protecting even babies. There is a rising pile of evidence that is being generated by dedicated and skilled scientists and the day is coming when medicine will have to face the truth and decide on a course of action. Let’s hope they will take a cue from the naturopath and the shaman, and that they will not put their hopes into a pill, but into the preservation of the balance of nature.

Be well,

Doc Griffith
———————————————————————————————————————————-
BMC Genomics. 2011 Apr 1;12:173.
Comparative genomic analyses identify common molecular pathways modulated upon exposure to low doses of arsenic and cadmium.
Benton MA, Rager JE, Smeester L, Fry RC.

BACKGROUND:

Exposure to the toxic metals arsenic and cadmium is associated with detrimental health effects including cancers of various organs. While arsenic and cadmium are well known to cause adverse health effects at high doses, the molecular impact resulting from exposure to environmentally relevant doses of these metals remains largely unexplored.

RESULTS:

In this study, we examined the effects of in vitro exposure to either arsenic or cadmium in human TK6 lymphoblastoid cells using genomics and systems level pathway mapping approaches. A total of 167 genes with differential expression were identified following exposure to either metal with surprisingly no overlap between the two. Real-time PCR was used to confirm target gene expression changes. The gene sets were overlaid onto protein-protein interaction maps to identify metal-induced transcriptional networks. Interestingly, both metal-induced networks were significantly enriched for proteins involved in common biological processes such as tumorigenesis, inflammation, and cell signaling. These findings were further supported by gene set enrichment analysis.
CONCLUSIONS:

This study is the first to compare the transcriptional responses induced by low dose exposure to cadmium and arsenic in human lymphoblastoid cells. These results highlight that even at low levels of exposure both metals can dramatically influence the expression of important cellular pathways.

Source:
Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.
Abstract

Khalil Gibran
On Work

You work that you may keep pace with the earth and the soul of the earth.
For to be idle is to become a stranger unto the seasons, and to step out of life’s procession, that marches in majesty and proud submission towards the infinite.
When you work you are a flute through whose heart the whispering of the hours turns to music.
Which of you would be a reed, dumb and silent, when all else sings together in unison?
Always you have been told that work is a curse and labour a misfortune.
But I say to you that when you work, you fulfill a part of earth’s furthest dream, assigned to you when that dream was born,
And in keeping yourself with labour you are in truth loving life,
And to love life through labour is to be intimate with life’s inmost secret.
But if you in your pain call birth an affliction and the support of the flesh a curse written upon your brow, then I answer that naught but the sweat of your brow shall wash away that which is written.
You have been told also life is darkness, and in your weariness you echo what was said by the weary.
And I say that life is indeed darkness save when there is urge,
And all urge is blind save when there is knowledge,
And all knowledge is vain save when there is work,
And all work is empty save when there is love;
And when you work with love, you bind yourself to yourself, and to one another, and to God.
And what is it to work with love?
It is to weave the cloth with threads drawn from your heart, even as if your beloved were to wear that cloth.
It is to build a house with affection, even as if your beloved were to dwell in that house.
It is to sow seeds with tenderness and reap the harvest with joy, even as if your beloved were to eat the fruit.
It is to charge all things you fashion with a breath of your own spirit,
And to know that all the blessed dead are standing about you and watching.
Often have I heard you say, as if speaking in sleep, “He who works in marble, and finds the shape of his own soul in the stone, is a nobler than he who ploughs the soil.
“And he who seizes the rainbow to lay it on a cloth in the likeness of man, is more than he who makes the sandals for our feet.”
But I say, not in sleep but in the over-wakefulness of noontide, that the wind speaks not more sweetly to the giant oaks than to the least of all the blades of grass;
And he alone is great who turns the voice of the wind into a song made sweeter by his own loving.
Work is love made visible.
And if you cannot work with love but only with distaste, it is better that you should leave your work and sit at the gate of the temple and take alms of those who work with joy.
For if you bake bread with indifference, you bake a bitter bread that feeds but half man’s hunger.
And if you grudge the crushing of the grapes, your grudge distills a poison in the wine.
And if you sing though as angels, and love not the singing, you muffle man’s ears to the voices of the day and the voices of the night.

Join Dr. Griffith at 7:30 on Wednesday, August 31st at the downtown Olympia Timberland Library for a talk on Traumatic Brain Injury and the Evidence of Treatment with DSMO!

Traumatic brain injury is a leading cause of death and disability. It is also a debilitating and heavily stigmatized condition that all too often goes undiagnosed and untreated leaving sufferers without hope of recovery. Current treatments work poorly, but Dr. Thomas Griffith, a local Naturopathic physician, administers DMSO, a compound made during the processing of tree pulp. Dr. Griffith is passionate about finding safe and effective treatments for serious conditions. He will present evidence from clinical trials that DMSO is such a therapy for severe traumatic brain injury. Dr. Griffith encourages anyone with TBI and their loved ones to come. Gulf War Veterans are especially welcome. Please tell anyone you know who might benefit from this information.

Location: Olympia Timberland Library

313 8th Avenue SE
Olympia, WA 98501-1307
360-352-0595
Age Group(s): Adults
Date: 8/31/2011
Start Time: 7:30 PM
End Time: 8:45 PM

Dr. Griffith practices at Vital HealthCare in Olympia, Washington. If you have questions, you can reach his office at 360-455-8281.

Vital HealthCare
3525 Ensign RD NE Ste N
Olympia,WA 98506
Phone 360-455-8281

Fermented Wheat Germ Bread Recipe:

!!THIS RECIPE IS NOT INTENDED FOR ANYONE WITH GLUTEN INTOLERANCE!!

Step 1: Fermented Wheat Germ

2 cups fresh raw wheat germ

1 ½ cups spring water

½ teaspoon of dry bakers yeast

Mix ingredients together in a bowl, cover and leave in warm place, about 85 degrees for 24 hours.

Step II: The Bread dough:

To the Poolish, add:

4 cups flour. A mixture of about half whole wheat and half unbleached white bread flour works well, but you can adjust the ratio to your personal preferences.  Or you can use spelt flour in place of the whole wheat flour.

1 1/2 cup water

mix until dough is formed. Let sit 20 minutes

then add :

1 Tbs sea salt or Celtic salt and knead until smooth and elastic, adding additional flour as needed.

Cover and let rise in warm place until doubled in bulk, 2-3 hours, divide in two, shape loaves, proof an additional couple of hours, again until doubled in bulk.  Bake in a hot oven, preheated to about 500 degrees, Once the bread is in the oven, reduce heat to 425 and bake until done.  The crust will be dark golden brown and sounds hollow when gently tapped.

If only cancer treatment could be as simple, and delicious, as eating a sandwhich on sourdough bread.  Well, maybe it is.  This article discusses “one of the most potent and best researched food supplements available for cancer patients” that you’ve never heard of… fermented wheat germ anyone?

Interestingly the discoverer of fermented wheat germ extract’s effect on cancer was Hungarian biochemist Albert Szent-Gyorgyi who received the Nobel Prize in Physiology or Medicine in 1937 for the discovery of vitamin C.  He observed that cancer rates were lower in people who ate whole grains vs. processed flours.  He hypothesized that compounds found in fermented bread might decrease cancer’s ability to utilize sugar and it now appears he was right.  It also has some potent effects on the immune response to cancer.  He believed in food as medicine and derived a recipe for bread made with fermented wheat germ, named “Poolish” (I know the name needs work) which now has been refined as an expensive product named Avemar.

It’s rare I get to tell patients to “eat their bread” but in this case, I think it is warranted.  I’ll be posting his recipe very soon so stay tuned…  Below are two abstracts summarizing some of the most up to date research. I encourage you all to google this yourselves or visit PubMed (http://www.ncbi.nlm.nih.gov/pubmed/) and see for yourself

Be well,

Doc Griffith

1.  Nutrition and Cancer

Volume 61, Issue 6, 2009

Avemar (Wheat Germ Extract) in Cancer Prevention and Treatment

András Telekesa, Márta Hegedűsa, Chang-Hoon Chaeb & Károly Vékeyc

pages 891-899

Available online: 10 Nov 2009

Abstract

“Many healthy foods are derived from wheat germ. The molecular composition of these products, however, greatly differs as shown by normal-phase HPLC-mass spectrometry analysis; thus, experimental data obtained by one of them is not necessarily true for the other. Avemar is a nontoxic wheat germ extract registered as a special nutriment for cancer patients in Hungary. It shows potent anticancer activity on cell lines by deeply interfering with glucose metabolism and affecting expressions of several kinases. In in vivo experimental models, Avemar is also effective by enhancing the activity of the immune system such as stimulating NK cell activity (by reducing MHC I molecule expression), enhancing TNF secretion of the macrophages, increasing ICAM 1 molecule expression on the vascular endothelial cells. All of these lead to apoptosis of tumor cells. The wide range of biological activity of Avemar probably cannot be explained by only one active ingredient. Since there are numerous experimental data and the clinical benefit repeatedly confirmed Avemar can be one of the most potent and best researched food supplements available for cancer patients”.

2. J Exp Clin Cancer Res. 2011 Apr 16;30:42.

Promising cytotoxic activity profile of fermented wheat germ extract (Avemar®) in human cancer cell lines.

Mueller T, Jordan K, Voigt W.

University of Halle, Department Internal Medicine, Oncology/Hematology and Hemostaseology, Ernst-Grube Str, 40, 06120 Halle/Saale, Germany. wieland.voigt@medizin.uni-halle.de.

ABSTRACT: Fermented wheat germ extract (FWGE) is currently used as nutrition supplement for cancer patients. Limited recent data suggest antiproliferative, antimetastatic and immunological effects which were at least in part exerted by two quinones, 2-methoxy benzoquinone and 2,6-dimethoxybenzquinone as ingredients of FWGE. These activity data prompted us to further evaluate the in vitro antiproliferative activity of FWGE alone or in combination with the commonly used cytotoxic drugs 5-FU, oxaliplatin or irinotecan in a broad spectrum of human tumor cell lines. We used the sulforhodamine B assay to determine dose response relationships and IC50-values were calculated using the Hill equation. Drug interaction of simultaneous and sequential drug exposure was estimated using the model of Drewinko and potential clinical activity was assessed by the model of relative antitumor activity (RAA). Apoptosis was detected by DNA gel electrophoresis.FWGE induced apoptosis and exerted significant antitumor activity in a broad spectrum of 32 human cancer cell lines. The highest activity was found in neuroblastoma cell lines with an average IC50 of 0.042 mg/ml. Furthermore, IC50-range was very narrow ranging from 0.3 mg/ml to 0.54 mg/ml in 8 colon cancer cell lines. At combination experiments in colon cancer cell lines when FWGE was simultaneously applied with either 5-FU, oxaliplatin or irinotecan we observed additive to synergistic drug interaction, particularly for 5-FU. At sequential drug exposure with 5-FU and FWGE the observed synergism was abolished.Taken together, FWGE exerts significant antitumor activity in our tumor model. Simultaneous drug exposure with FWGE and 5-FU, oxaliplatin or irinotecan yielded in additive to synergistic drug interaction. However, sequential drug exposure of 5-FU and FWGE in colon cancer cell lines appeared to be schedule-dependent (5-FU may precede FWGE).Further evaluation of FWGE as a candidate for clinical combination drug regimens appeared to be warranted.

NIACIN AIM HIGH TRIAL STOPPED DUE TO LACK OF BENEFIT IN CARDIOVASCULAR EVENTS.

Recent halting of the AIM HIGH trial investigating Niacin’s ability to prevent cardiovascular risks is calling into question the benefit of high dose niacin. On Thursday 5/26/11 the National Heart, Lung, and Blood Institute of the National Institutes of Health stopped a trial of 3414 subjects on Niacin after 32 months, 18 months prematurely. The NIH stated, that in conjunction with statin treatment, high dose niacin to raise HDL (“good cholesterol”) and control triglycerides, “did not reduce the risk of cardiovascular events, including heart attacks and stroke”. Low HDL, high LDL (“bad cholesterol”) and high triglycerides are predictors of greater risk. Niacin does successfully lower triglycerides and raise HDL. Research has yet demonstrated that raising HDL will reduce adverse cardiovascular events.This study was supposed to do so definitively, and failed. The niacin plus statin drug treatment group experienced no reduction in heart attacks, acute coronary syndrome or procedures to improve blood flow; In fact a slight (%1.6) increase in stroke was seen.

At this point no new guidelines about the use of Niacin for high risk patients have been announced. There are always confounding factors in research, and that’s one reason why Naturopathic physicians depend on a more individualized and constitutional approach with patients. So before tossing out your Niacin, it’s important to remember the devil is always in the details. There will be an in-depth review of AIM HIGH before insights can be teased out to dictate new clinical standards and direct future research. The patients in AIM HIGH were 64 years old on average, had history of previous cardiovascular disease, suffered from metabolic syndrome or diabetes, and were hypertensive, with high triglycerides, low HDL and their LDL levels were already lowered to 40-80 by intensive statin dosing. These criteria leave a number of details unaccounted for and raise a new set of questions. Fortunately there is a large international trial of high dose niacin ongoing which will hopefully elucidate AIM HIGH’s findings.
There is always a substantial lag between research and change in clinical practice that leaves physicians to extrapolate and derive a sensible approach. As a physician I would like to someday know the answers to the following questions:

1. What about younger and healthier patients?
Is it possible that younger patients with elevated LDL and triglycerides, low HDL levels, and without pre-existing cardiovascular disease, might still benefit preventively by taking Niacin to lower triglycerides and boost HDL?

2. Was blood sugar control factored in?
Given the contribution of diabetes to adverse cardiovascular events, were these factors well accounted for during AIM and if so could they have altered the outcome? Diabetes increases risk greatly beyond its association with lipid levels. Diabetes increases oxidation and inflammation systemically.

3. Is the LDL cholesterol hypothesis (LDL causes heart attacks) a bit oversimplified and outdated?
Researchers are making huge strides towards unraveling the complexities of other lab markers for cardiovascular risk like lipoproteins, apolipoproteins, inflammatory and oxidative markers, subtypes of HDL and LDL, phospholipase, coagulation indices… etc. It’s becoming obvious that there is way more to the story and yet clinical practice standards have not kept up. The standard LDL hypothesis fits the standard Statin paradigm so well that there is le$$ incentive to figure out if LDL reduction is the best way to decrease cardiovascular risks.

4. What about inflammation?
Statins have potent anti-inflammatory and anti-oxidant properties. Since the control and niacin group both got statins, this study may demonstrate that controlling inflammation and oxidation is as effective as controlling levels of LDL, HDL, and Triglycerides to reduce cardiovascular events. Since the LDL hypothesis of heart disease is thoroughly entwined with statin recommendations there is a lack of financial incentive or resources to do this research.

5. What to do now about triglycerides and HDL?
The findings of this study leave no evidence based pharmaceutical option for patients as past trials have all failed. Drugs like Tricor (fenofibrate), Zetia / Vytorin and torcetrapib don’t help either as their trials have already shown.
*The fanatical emphasis on pharmaceutical interventions for heart disease neglects the crucial role of diet and exercise in protecting patients against cardiovascular diseases. These approaches are foundational and are typically the last and most briefly covered in studies and in the office visit. The assumption is that patients won’t change, so it’s no wonder many don’t, and cardiovascular disease continues to reign as America’s top killer.

6. How about Omega 3’s like EPA and DHA?
There is already a prescription called Lovaza which is essentially concentrated EPA and DHA at high dose. Of course it’s more expensive than just buying fish oils at a supplement store and insurance companies won’t typically cover it, but it does effectively control elevated triglycerides, raises HDL, prevents oxidation of LDL, helps stabilize blood sugar, decreases inflammation and reduces clot formation and more. It has also been shown to independently reduce the risk cardiovascular events in 3 large controlled trials of 32,000 participants. It’s also interesting to note that fish oils decrease risk despite modestly increasing LDL cholesterol…

In summary:

I can only wish that someday the foundation of cardiovascular prevention will be laid where it belongs, grounded on exercise and diet (a little love is also great for the heart of course). I am lucky to be part of a profession that also focuses on enhancing health, not merely suppressing symptoms or lab values. As a naturopath, I can utilize a multitude of options for my patients and actually help them understand their own potential to reach optimal health. As for the AIM HIGH trial, it only reaffirms my commitment to true prevention. I await further news – stay tuned, take your fish oils, eat a big salad and go take a walk outside with a loved one.

Be well,
Doc Griffith