DISCUSSION EXAMPLE OF GOVERNMENT/VA/NAS-IOM BIAS
Normally I use “peripheral neuropathy (PN)” as a primary example of “government bias” against our Nations Veterans as most of you that have followed my issues have seen. That particular disorder has an even more obvious government/VA bias in that our “honorable government” put a time limit on not only the manifestation but also the damage to the nerve myelin matter would repair itself within two years after removal from the toxic chemicals.
This is total “government/VA bureaucracy science based on dollars” not actual medical or scientific science or even statistically that can be proven.
This would have to conclude that somehow our government/VA/NAS-IOM has magically defined the following:
Rate of exposure to manifest this medical disorder.
Minimum body threshold to create this medical disorder.
Since a time limit is put on the manifestation of the medical issue, the actual causation at root cause failure must have clearly defined medically to the dioxin, TCDD.
Since a time limit is put on the resolution of the medical issue, the actual causation at root cause failure levels and the methodology of how removing ones self from the toxic chemical exposures will allow the medical disorder to resolve itself; must be identified and understood by someone or some scientists. (i.e. once removed from the toxicant the damaged myelin nerve matter, axons will regenerate.)
All of the above is based on the nerve damages “not being caused” by a secondary response such as a disturbed immune system in long-term damages such as a form of immunotoxicity or neurotoxicity damages.
Therefore, some one somewhere has determined that direct contact with the dioxin, TCDD at some level will create some level of “direct peripheral nerve damage only” that does not involve a central nervous system involvement and they know how it does it and what the ingestion rate must be and/or the total body threshold is regardless of method of ingestions.
This scenario is just government/VA/NAS-IOM hocus pocus scientific conclusions.
This scenario might fit the causation of PN by Dapsone, noted for PN causations but certainly not the toxic chemical dioxin, TCDD or any of the other toxic chemicals from secondary development causations.
While the contrary can be proven to medical, science, or even statistically the levels required for compensations for this debilitating disorder and has been proven to p-values of 0.039 associated to Vietnam Veterans exposure to the dioxin, TCDD and p-values of difference to p - 0.0042. As well as these medical issues were found in toxic chemical victims going back to the late 1940’s. Including our own Ranch Hand study found a direct response to the dioxin, TCDD and PN in their test cohort’s decades after our war.
This also includes the Chronic Fatigue Issues that go with this nerve disorder also found in exposure victims even in our own government studies that just as likely as not associated to Central Nervous System damage associated with Chronic Fatigue Immune Dysfunction Syndrome, or sometimes called Myalgic Encephalopathy.
This seems to be located in dorsal root ganglionitis (inflammation in the spinal cord) - recently discovered in a two-week autopsy, with the cause of death listed as Chronic Fatigue Syndrome. This becomes a “clear physical manifestation” of the disease.
This new finding seems to confirm what many scientists have been saying for decades now regarding PNS issues and that is before any PNS issues manifest a CNS subclinical event/causation has taken place and precedes any PNS manifestations.
While there seems to be, a running battle between psychiatrists and medical doctors as to the cause of this disorder. It seems there is a biological issue associated to our toxic chemical exposures in our damaged immune systems that create this nerve damage or inflammation as well as the chronic fatigue issues found in 1984 by our own governments studies of those that sprayed the toxic chemicals.
Veterans this nerve damage pain is not just in your mind, as some doctors would say. It actually hurts and there is little any doctor can do except try and control the symptoms. The damage is autoimmune and there is little that can be done.
Immune system disorders in our Vietnam Veterans has even been found by our “own government studies.” In many other studies, these overactive as well as confused immune system responses were found.
Yet, is still ignored by our Government/VA/ and its contracted agencies that determine our Veterans fate in the impacts to diseases and disorders relating to disability and death.
This subject will be covered in my failure discussion I am working on now down to the immune system cytokine level. As well as the known fact that the dioxin, TCDD seeks out for repository a lipid environment. Our central nervous system is 70-80% lipids (fat) with the rest made up by proteins.
Christ almighty folks that is how they check our guys for residual dioxins by examining fat tissues 40 years after the exposures. The toxicant is still there!
To now say this toxic chemical substance cannot and will not seek the central nervous system is somewhat biased, based on government mandated results - not facts.
The EPA’s dioxin experts in 2005 put out even more compelling data that shows a direct ratio of ng/kg dosing. This is certainly more realistic on a toxic chemical issues as to disorders or types of disorders than just a parts per trillion (ppt) or parts per billion (ppb) or even parts per million (ppm) because it looks at the victims mass per toxic chemical exposures.
This new data also indicates significant correlation that the 1994 EPA’s dioxin reassessment was right on track just like it was in 1979 when the EPA shelved the reports and never released them. Our EPA clearly has the most data on dioxins and dioxin like PCB’s yet our government pays over 300 million dollars on studies they can control, manipulate, and stall data verification for decades.
The EPA on “Dioxins’ Effects in People”(2005):
Biochemical effects can impact any of the body’s system in many systemic medical issues.
Altered Sex Ratio (Indicated the greatest contributing factor was “paternal exposures”)
Delayed Breast Development
One of the findings, which I have repeated time and time again to our congress and they do nothing for us, is this Body Burden to create a cancer versus an Immune System Issue. The EPA has indicated in their charts of Body Burden versus Dioxin effects ng/kg of 1.6 for adult immunotoxicity. With the exception of CYP1A1 (P450) induction changes immunotoxicity minimum is the smallest ng/kg body burden. Yet, Veterans according to our Congress – VA –NAS/IOM says that the lowest exposure causation cannot be associated to those that wore a Military Uniform and their toxic chemical exposures. Make any sense? Of course not. A ninth grade math student could figure this government collaboration out in which the "least exposed" would be the most prevalent. Yet, our congress sits blind, deaf, and dumb to the suffering of government caused issues to the Nations Veterans.
Two sensitive areas subject to dioxins are reproductive toxicity as well as adult immunotoxicity. Also clearly showing the body burden required versus the current average. Of course, there are very few if any Vietnam Veterans that will meet the current average in populations. These data points clearly indicate the most sensitive of adverse affects discussed above. These data points also indicate that our associated cancers already associated require a body burden much much greater than that of immune system issues or reproductive issues.
Yet, the IOM and the VA still refuse to admit such dioxin caused disorders in our Veterans even though there are presumptive exposures to unprecedented toxic dioxin, TCDD strengths and application of dose rates.
This nothing short of total government biases in directed philosophy against the Veterans as well as their families.
A nanogram is one billionth of a gram.
A kilogram: standard SI unit of mass. Approximately 2.2 pounds.
Here is another specific disorder to discuss that was found associated to dioxin levels in our VETERANS –
“increase in triglycerides.”
While this sounds SIMPLISTIC and harmless, it is far from it.
A found relationship between increased triglyceride levels and dioxin levels was found. (1999 August RANCH HAND Transcripts)
The Ranch Hand veterans with the highest combination of initial dioxin level (>94 ppt) and 1987 dioxin level (>10 ppt) had elevated triglyceride levels in 1997 (118.2 mg/dl versus 105.9 mg/ dl in comparison veterans, p= .01). The longitudinal analysis also revealed that this category of Ranch Hand veterans experienced the largest increase in triglyceride levels over the 15-year follow-up (+13.1 mg/dl versus +1.3 mg/dl in comparison veterans, p = .02). (2000 Update from the government contracted NAS/IOM)
Other studies have found these facts as well.
Just for talking purposes lets say the above findings by our own government studies as well as the government contracted and paid for agency found this dioxin association to an increase in triglycerides to at least those certainly at the highest levels of exposures as stated above. Also bearing in mind this form of exposure is the most benign form of exposures. Skin absorption is limited and slow but dioxins are absorbed well in the GI tract and lungs. Dioxins lodge in the liver and fat cells.
This is also a government/VA mistaken directed philosophy that those that sprayed the toxic chemicals would be the worst off of all the Vietnam Veterans. Of course, this is flawed philosophy since rate of ingestion and method of ingestions to toxic chemicals does have a role in the severity of the disorders and what disorders will develop.
Now lets consider what are the medical impacts to the Vietnam Veteran long term from an increase in triglycerides as we see above categorically identified above.
Again, sounds simplistic but what are the trends and medical markers for the patient who has developed hypertriglyceridemia or an increase in triglycerides, regardless of causation.
How is an excess of triglycerides
“Excess triglyceride in plasma is called hypertriglyceridemia. It's linked to the occurrence of “coronary artery disease.” Elevated triglycerides may be a consequence of other disease, such as untreated diabetes mellitus.
An increase in triglycerides can also represent an on-going chronic or acute phase inflammatory condition. This is phasing is partially verified by another blood test called a C reactive protein test. (I could find no such reference to this test in the Ranch Hand transcripts and none mentioned in the IOM report as it relates to the possible long-term effects of the stated found dose response to the increased triglycerides in long-term health.)
The CRP test is sometimes used in patients with inflammatory bowel disease and some forms of arthritis and autoimmune diseases to assess how active the inflammation is and to monitor the treatment. The CRP test is also used to monitor patients after surgery or other invasive procedures to detect the presence of an infection during the recovery period. CRP tests are not specific enough to diagnose a particular disease. Rather, CRP is a general marker of infection and inflammation that alerts medical professionals that further testing and treatment may be necessary.
Since the CRP is a general test, a positive CRP may indicate a number of things, including:
Connective tissue disease
Bacterial, viral, fungal, or parasitic infection
Other causes of ongoing inflammation
Is HS-CRP a real risk factor such as cholesterol and high triglycerides?
In studies involving large numbers of patients, CRP levels seem to be correlated with levels of cardiac risk. In fact, CRP seems to be at least as predictive of cardiac risk as cholesterol levels. Data from the Physicians Health Study, a clinical trial involving 18,000 apparently healthy physicians, found that elevated levels of CRP were associated with a threefold increase in the risk of heart attack.
In the Harvard Women's Health Study, results of the CRP test were more accurate than cholesterol levels in predicting coronary problems. Twelve different markers of inflammation were studied in healthy, postmenopausal women. After three years, CRP was the strongest predictor of risk. Women in the group with the highest CRP levels were more than four times as likely to have died from coronary disease, or suffered a nonfatal heart attack or stroke. This group was also more likely to have required a cardiac procedure such as angioplasty or bypass surgery than women in the group with the lowest levels.
Elevated hs-CRP is no doubt to anyone; except the Ranch Hand, NAS/IOM, and our government; related to increased risk for heart attack, restenosis of coronary arteries after angioplasty, stroke, and peripheral vascular disease (PVD).
I would think that any Vietnam Veteran demonstrating this increase in triglycerides regardless of cholesterol level is at long-term toxic chemical causation risk for vascular and heart issues. If the C-reactive protein test also shows this ongoing inflammatory marker, this becomes just more evidence as to the increased risk factors from the toxicant causation.
In lab work for this test and phasing the disorder the following is stated:
HS-CRP in mg/L normal listed as 0-5
Notes associated to this test:
C reactive protein (high sensitivity) can be used to monitor risk of cardiovascular and peripheral vascular diseases. The same assay can also be used to assess inflammation.
Interpretive ranges are as follows:
75% of CRP levels in healthy adults are <3.2 mg/L in published studies.
Values in the upper quartile of reference range >3.2 mg/L are associated with increased cardiovascular risk.
Single measurements may not reflect true baseline CRP levels.
Values >5 are suggestive of acute phase response and may be seen in acute illness.
Just for info, mine was 7.1 mg/L along with increased triglycerides since 1982 and the VA seems to think this is not an issue medically nor is it associated to wartime service in a toxic chemical environment. This along with about four antibody issues that directly correlate to toxic chemical exposures proven in many studies including our own government studies.
Hypertriglyceridemia is a disorder in which the concentration of very low density lipoprotein (VLDL) is elevated in the plasma. This leads to increased risk of heart disease, obesity, and pancreatitis.
May manifest as premature coronary artery disease.
Signs and tests
The goal of treatment is to control exacerbating conditions, such as obesity, hypothyroidism, and diabetes wherever possible. Alcohol use should be discontinued. Oral contraceptive use should be reviewed and the specific type chosen carefully. Restriction of excess calories and reduction of saturated fats in the diet is indicated.
If high triglyceride levels persist with maximum dietary treatment, drug therapy should be started. Nicotinic acid or Gemfibrozil are drugs that have effectively reduced triglycerides in people affected with hypertriglyceridemia.
There is an increased risk of coronary artery disease and pancreatitis with this disorder. Weight loss and control of diabetes has a positive effect on the outcome.
increased risk of pancreatitis
increased risk of coronary artery disease
Now lets look at what the government contracted NAS/IOM – government controlled Ranch Hand connection says regarding this issue and the seemingly lack of concern as to this data as it relates to the already found ischemic heart disease, stroke, atherosclerosis, and peripheral artery disease (PAD) found in about every study I could review including the Ranch Hand transcripts that shows a significant connection to cardiovascular mortality complications as a result from exposures to the dioxin, TCDD.
If there are 10 studies that show the issue walks like a duck and talks like a duck chances are it is a duck and is associated unless our government is involved.
Where do we find government biases as well as NAS/IOM government contracted biases?
See individual numbers below.
(1) The Ranch Hand data was for total cholesterol, HDL cholesterol, and triglyceride levels. If one were really looking, at the data for a connection to the already known increase in Ranch Hand mortality from cardiovascular failures then obviously VLDL or LDL should have been the test to examine, not HDL. HDL is good and the higher the number the better. The HDL cholesterol while nice has little to do with the disorder. You can have a good HDL number and have a horrible LDL and or VLDL numbers and you still have a problem. Yes, you need to keep this number as high as possible but there are two separate drugs that do that. One for raising good cholesterol and one for lowering bad cholesterol. Although just recently there are a few combinational drugs that will try and do that in raising one while lowering the other. Therefore, comparing HDL is like saying the dioxin while causing no harm in this good cholesterol - it did not increase it as if dioxin, TCDD were good for you either. In other words, what this statement by the IOM indicates is do not use dioxin, TCDD to raise your HDL. In any failure analysis, one must use worst-case failures not best-case failures. Total Cholesterol means very little - Example – many patients can have a total number within range and yet the well being of cholesterol in HDL, LDL, VLDL as well as triglycerides is skewed. A high LDL level (more than 160 mg/dL or 130 mg/dL or above if you have two or more risk factors for cardiovascular disease) reflects an increased risk of heart disease. What would have been nice here if the Ranch Hand had given the IOM the data and I assuming they did not since the IOM did not report or analyze the increase in triglycerides found in the worst exposed and a comparison of LDL or VLDL cholesterol which would be more of a positive marker for things to come in long term damages such as any form of heart or vascular complications. Including PAD and even brain atrophy and brain infarction (associated with strokes) at an early age, also found in studies associated to the dioxin, TCDD.
Now for those that would say, well the increase in triglycerides was found because of the untreated diabetes. Not so. If you believe in mathematics and the statistical formulas used to determine the risks and statistical issues. Diabetes was found at a p-value of p - 0.0230. Some of these cardiovascular connections such as vasculopathy were found at a p-value of p – 0.0002. Pretty much concludes this is not just a cohort coincidence.
I again question the IOM and/or the input to them from the Ranch Hand or lack of input as to the triglycerides and LDL or VLDL. That is the key to diagnosis and predictors of long-term inflammatory damages found the found data points specifically related to the dioxin, TCDD.
The lack of these tests results and the lack of the C-reactive protein tests certainly are questionable even to the novice researcher considering the following:
Testing for C-reactive protein may be a good way to keep tabs on the inflammation that causes heart attacks.
Since the mid-1990s or so, researchers have changed the way they look at atherosclerosis. They use to regard it as a gradual buildup of fat- and cholesterol-filled plaques inside arteries. Now they see an inflammatory process that sometimes has a nasty, volcanic climax: A plaque ruptures, spilling its contents into the bloodstream, causing a potentially fatal traffic jam of blood clots and other factors.
This new view of atherosclerosis has doctors hunting for ways to detect inflammation early. So far, the strongest candidate is C-reactive protein (CRP).
Researchers use to think that CRP was made only in the liver. Now they know that it’s also made within the coronary arteries that carry blood to the heart. The test for measuring CRP produced in these coronary arteries is called a “high-sensitivity CRP” test or hs-CRP for short. In 2003, the American Heart Association endorsed the use of hs-CRP for people at intermediate risk for heart attack.
Now the IOM and the Ranch Hand seemed to have latched on to this high triglycerides and a must find for high cholesterol for any association to cardiovascular disorders. Not so!
In one study, patients who ended up with low LDL and CRP levels were less likely to have serious heart problems than those who had low LDL but “high CRP.”
The results suggest that CRP levels do matter and that doctors may need to have two goals in treating heart attack patients with statins: getting the LDL below 70 mg/dL and the hs-CRP level below 2.0 mg/L.
In the other study, researchers used ultrasound to measure the growth (“progression”) of atherosclerotic plaque among heart disease patients taking the same statin drugs. The researchers found a relationship between decreasing CRP and a slower progression of atherosclerosis. In fact, among those who had both low LDL and CRP, the plaque actually got smaller.
The test is not a replacement for cholesterol testing but something to be used in addition. Remember that half of all heart attacks and strokes occur among those with normal cholesterol levels, so knowing cholesterol may not be enough. The high-sensitivity CRP test may be particularly useful for people with metabolic syndrome; a condition that includes elevated blood glucose levels, high triglycerides, and several other risk factors.
The bottom line to tie the triglyceride increase to only cholesterol is not scientific and biased against finding for the Veteran and an inflammatory vascular state. To focus on the one issue and deny connection based on an unrelated issue is even more biased. One must take all the issues of the data point. That includes all system impacts not just the ones you can make a case for denial.
The Ranch Hand transcripts also discussed this X-factor or metabolic syndrome that seemed to correlate with the Ranch Hand cohorts.
What is this metabolic syndrome or X-factor associated with hyperlipidemia?
The metabolic syndrome is characterized by a group of metabolic risk factors in one person. They include:
Abdominal obesity (excessive fat tissue in and around the abdomen)
Atherogenic dyslipidemia (blood fat disorders — high triglycerides, low HDL cholesterol and high LDL cholesterol that foster plaque buildups in artery walls)
Elevated blood pressure
Insulin resistance or glucose intolerance, the body can’t properly use insulin or blood sugar. (It should be noted here the VA refuses to test using the more sensitive oral glucose test or to compensate or treat the glucose intolerance. Yet, clearly with the other factors found this is indeed all related to the exposures and levels of exposures.
Prothrombotic state (e.g., high fibrinogen or plasminogen activator inhibitor-1 in the blood) (It should be noted here the test for high fibrinogen was brought up in the Ranch Hand transcripts but there was no follow-thru that I could find that this test was used on the cohorts to establish this “inhibiter-1” issue in the blood.)
Proinflammatory state (e.g., elevated C-reactive protein in the blood)
People with the metabolic syndrome are at increased risk of coronary heart disease and other diseases related to plaque buildups in artery walls (e.g., stroke and peripheral vascular disease) and type 2 diabetes.
Proinflammatory state. A proinflammatory state is recognized clinically by elevated C-reactive protein levels. It is commonly present in patients with the metabolic syndrome. This may be because excess adipose tissue releases inflammatory cytokines that may elicit higher CRP levels.
Prothrombotic state. A prothrombotic state characterized by increased plasminogen activator inhibitor 1 and fibrinogen also associates with the metabolic syndrome.
In reading the EPA’s 2005 update, I noticed some indicators of involvement in dioxin disorders in the cytokines IL-6 and IL-1 beta as well as Tumor Necrosis Factor (TNF). I knew about the TNF but was unaware of the other Interlukins. Outside of IL-4 and IL-10, that was found, upregulated in Vietnam Veterans.
I sent an e-mail requesting where this data came from and sort of found IL-6 myself as to its involvement with dioxin effects. It seems IL-6 is associated with several effects one of which is prothrombotic state referenced above in the metabolic syndrome as well as C-reactive protein.
Indexes of inflammation are related to indexes of the prothrombotic state and may be related to the clinical variables of the patients (underlying vascular disease and co-morbidities), rather than simply to the presence of Arterial fibrillation (AF) itself.
It also seems there is a proinflammatory response to changes in IL-1 also.
More details on this subject and cytokine involvement later in my report in work.
It is any wonder the Ranch Hand found increased cardiovascular mortality and arterial issues as well as the 2003 Korean Agent Orange Impact Studies found ischemic heart disease, vasculopathy, peripheral vasculopathy, and valvular heart disease.
The question must be asked; how many Veterans would still be alive today had they and their doctors been told early on by our own government what to look for in something as simple as increased triglycerides that did not correlate to any known issues or testing correlation and had started treatment in the 80’s.
(2) This is the classic way of introducing more and more categories that are subjective in what they even mean and very subjective as to what numbers are used in the formulas in calculating the results. This introduces more and more cumulative errors in the results. They adjusted for age, race, military occupation, current and lifetime alcohol use, and history of industrial or degreasing chemical exposure.
Certainly age may have something to do with this disorder but one would wonder if that difference would have been valid had the tests have been done in 1979 instead of 20 years later while our government stalled doing anything and does this age issue apply in our fellows that were more than likely in their late 40’s. I would say an increase in mortality and disease development in cardiovascular issues at an average age of late 30’s to late 40’s or early 50’s is just a little outside of the normalized population.
Certainly, race plays a part as that is the human genotype normalization and is more than likely studied and data gathered for centuries. Assuming the correct adjustment was used in our government controlled study and not applied with a heavy hand to change the results.
I would have to wonder why military occupational specialty has any form of failure analysis since “contamination is contamination” it does not matter if you were a 13A10, 17H20, or a civilian walking through the area. The study was supposed to be taking fat tissue samples and analyzing the residual dioxin, TCDD found attached. This would lead anyone to believe this is just another error rate introduced for nothing but bias to skew numbers. These were not exposure assumption rates based on MOS but actual measurement regardless of what job you had or what rank you were or if you were enlisted or officer. I doubt if dioxins know the difference between an enlisted body/blood versus an officer’s body/blood. Congress has great power but that is outside of their god like powers.
One of my major concerns when I found out the cohorts were those that served in OPERATION Ranch Hand and a comparison group of Vietnam Veterans. I asked the IOM how in the world does this study prove anything since the p –values of difference would be minimized as to any effect of “serving in Vietnam” and the effect of “the many different chemicals used” would be minimized. That is when I realized they were only doing dioxin only samples and picking an arbitrary and subjective cut off of body burden to even associate any disorders to the dioxin, TCDD only. So the p – value of differences are minimized anyway. No exclusionary testing was being done as to the possibility of other chemicals causing many of the overlapping symptoms. The study seems to very one sided anyway and in some areas cannot even verify issues found associated to dioxin, TCDD. Trends maybe; but not the proof of failure cause, as the study seems to suggest it is doing.
However, if you now minimize even more by using some issues like being an officer versus an enlisted man; or using some sort of MOS set aside category then the whole premise of sampling is bogus. I have no problem with this if they wanted to do the subcategories as some sort of “additional information (lets look and see)” but to use that in study data to another government contracted agency that is supposed to review their work and make critical path decisions to provide “service connected medical health care” or “disability/mortality compensations” then this premise and protocols seemed to be totally biased one way.
Current and lifetime alcohol use is also suspect since there are millions of heavy drinkers in our nation that do not die in their late 30’s to late 40’s to early 50’s from cardiovascular failures. I would question what numbers were being biased in the failure analysis and based on what consumption.
History of industrial or degreasing chemical exposures is another one that seems illogical as a failure model unless where the Veteran worked and its employees were tested as to some form of accumulation of dioxin, TCDD. If this was not done then once again an assumption has been made to the detriment of the Veteran’s.
While it was not mentioned here by the IOM, even things around the family household were also thrown into the mix by the Ranch Hand study. This was additive but no proof of any effect or impact, merely assumptions.
We know there are studies that show a 12% increase in all cancer sites alone when doubling the background from 5 part per trillion to 10 parts per trillion. To not conclude that doubling the background for heart issues and vascular issues is the same or even worse is somewhat suspect, especially in long-term issues, >20 years.
This is even more obvious when one looks at the Seveso, Italy dioxin study that shows more mortality from ischemic heart disorders than from any cumulative cancer totals. (160 to 179) The Risk Ratio in heart issues while not significantly higher than cancers was found higher in zones A + B (the highest level of exposures). Moreover, when one looks at the vascular p-values found in the Korean study it indicates many cardiovascular separate issues found at <p - 0.05. The trends and findings are obvious.
Yet, neither the Ranch Hand nor the IOM seemed to want to conclude any increase in cardiovascular issues that would be directly related to the found dioxin response to an increase in triglycerides and metabolic syndrome.
(3), (4), (5), and (6) I have no clue what the NAS/IOM was trying to convey here. It is almost like they are trying to just fill up the paper with nonsense and data that means nothing. No analysis or concern as to the LDL levels or VLDL levels only HDL levels and some sort of denying any associations to the good cholesterol and increase in triglycerides found. Then it states some fat analysis was done which would indicate they were only looking an increase in fat or weight associated to the increase. As if skinny folks do not die from “cardiovascular issues” with an increase in triglycerides. These scientists are so focused on presenting what is not associated they cannot see the Veterans forest is dying from cardiovascular dioxin caused issues. Yet clearly when these totally biased statements were made they knew of the increase of cardiovascular issues already found at least as far back as 1991.
Lets cover up an eye and only look at specific issues as it relates to one thing, not the many other things in total that could be caused or associated.
The finding of increased triglycerides seemed to not be a concern since “HDL cholesterol levels” did not seemed to be associated or track the same progression nor did the total cholesterol. Yet, the medical concern should be increase in triglycerides with an increase in LDL and/or VLDL as the marker for cardiovascular disorders and this was never mentioned nor determined.
Yet, I would bet if you went back an looked at the gathered test data you would see that an increase in triglycerides (a form of fat) started early on as a precursor to these cardiovascular issues including PAD and should have been treated regardless if you have a cholesterol ratio issue or not!