Urinary 6-Sulfatoxymelatonin (MT6s) is the main metabolite of melatonin.

Melatonin assists in the body’s sleep/wake cycle and is also a very powerful antioxidant. Primary production is in the pineal gland. The GI mucosa is a significant source secondary production, with retina, bone marrow, platelets, skin, and lymphocytes all producing smaller amounts. GI-produced melatonin has paracrine effects (=affects adjacent cells) and does not enter general circulation. MT6s itself has no physiologic activity, but is a good indicator of whole body melatonin production. Low urinary MT6s is an indication for melatonin supplementation. It is normal to see elevated urinary values with supplemented doses higher than 1mg.

Two types of antibodies are detected in the Western blot test.

This particular marker is called 66 KD (IGG) Band and hence is a IgG antibody marker. IgG antibodies are a sign of an older infection. In contrast, IgM antibodies reflect a relatively recent infection. 

IgM antibodies usually disappear after eight weeks post-exposure. 
IgG remains in the serum for a very long time. 

7-keto DHEA (also known as 7-oxo DHEA) is a steroid produced by metabolism of DHEA.

It is not directly converted to testosterone or estrogen.

7-keto DHEA is rapidly absorbed when given as a supplement and converted to its sulfate derivative. It is commonly used to produce the metabolic effects of DHEA while avoiding metabolism into estrogens or androgens, and clinical research supports its role in benefiting metabolism and weight management. Endogenous 7-keto DHEA may have some anticortisol activity through enzyme competition which in the case of hypercortisolism may be beneficial to the adverse effects of cortisol on metabolic syndrome. Most studies on 7-keto DHEA are on improving the metabolic rate where there appears to be improvement in metabolism despite being on a low caloric diet. There is also limited information that 7-keto DHEA may act to increase levels of T3 while patients are on a caloric restricted diet.

8-hydroxy-2-deoxyguanosine measures the oxidative impact to DNA. 8-hydroxy-2-deoxyguanosine levels will be high if your total antioxidant protection is inadequate.

8-hydroxy-2-deoxyguanosine measures the oxidative impact to DNA. 8-hydroxy-2-deoxyguanosine levels will be high if your total antioxidant protection is inadequate.

8-hydroxy-2-deoxyguanosine measures the oxidative impact to DNA. 8-hydroxy-2-deoxyguanosine levels will be high if your total antioxidant protection is inadequate.

8-hydroxy-2-deoxyguanosine measures the oxidative impact to DNA. 8-hydroxy-2-deoxyguanosine levels will be high if your total antioxidant protection is inadequate.

8-hydroxy-2’-deoxyguanosine is marker resulting from DNA damage due to oxidative stress.

8-hydroxy-2’-deoxyguanosine (8-OHdG, or 8-oxodG) is a marker of oxidative stress. Urinary 8-OHdG, in particular, has been measured most frequently to indicate the extent of oxidative damage. guanine is most prone to oxidation. Guanine molecule, one of the four main nucleobases found in the nucleic acids DNA, oxidizes to produce the modified 8-OHdG which acts as one of the predominant forms of free radical-induced lesions of DNA. Oxidative modified DNA in the form of 8-OHdG can be quantified to indicate the extent of DNA damage

8-hydroxy- 2’-deoxyguanosine (8-OHdG) is a byproduct of oxidative damage to guanine bases in DNA. It is used as a biomarker for oxidative stress and carcinogenesis.

It has been studied to estimate DNA damage after exposure to carcinogens including tobacco smoke, asbestos fibers, heavy metals, and polycyclic aromatic hydrocarbons.

8-OHdG levels are positively associated with markers of inflammation and evening cortisol, indicating that increased physiological or psychosocial stress is associated with increased oxidative damage.

8-hydroxy- 2’-deoxyguanosine (8-OHdG) is a byproduct of oxidative damage to guanine bases in DNA.

It is used as a biomarker for oxidative stress and carcinogenesis. It has been studied to estimate DNA damage after exposure to carcinogens including tobacco smoke, asbestos fibers, heavy metals, and polycyclic aromatic hydrocarbons.

8-OHdG measures the effect of endogenous oxidative damage to DNA. The marker is used to estimate the risk for various cancers and degenerative diseases. Adjusting treatments and lifestyle to minimize the presence of 8-OHdG is a productive step toward health and longevity.

8-OHdG measures the effect of endogenous oxidative damage to DNA. The marker is used to estimate the risk for various cancers and degenerative diseases. Adjusting treatments and lifestyle to minimize the presence of 8-OHdG is a productive step toward health and longevity.

Two types of antibodies are detected in the Western blot test.

This particular marker is called 93 KD (IGG) Band and hence is a IgG antibody marker. IgG antibodies are a sign of an older infection. In contrast, IgM antibodies reflect a relatively recent infection. 

IgM antibodies usually disappear after eight weeks post-exposure. 
IgG remains in the serum for a very long time. 

Low a-1 level is a significant predictor of recurrent CVD events.

The marker α-1 from the Boston Heart HDL Map test is a key player in understanding cardiovascular health. HDL, or high-density lipoprotein, often called "good cholesterol," helps carry cholesterol away from the arteries to the liver, where it can be removed from the body. Among the different types of HDL, α-1 is the most mature and efficient at clearing cholesterol from the bloodstream. When levels of α-1 HDL are low, it’s a red flag because it significantly increases the risk of recurring heart problems.

The α-2 marker, one of the key HDL subpopulations measured by the Boston Heart HDL Map® test, plays an important role in assessing cardiovascular health. HDL, or high-density lipoprotein, is commonly known as "good cholesterol" because it helps remove bad cholesterol from the bloodstream. The α-2 HDL subclass is a specific type of HDL particle that carries cholesterol away from the arteries and back to the liver, where it can be processed and removed from the body. Measuring the levels of α-2 HDL can provide valuable insights into an individual's risk for cardiovascular disease (CVD).

The marker α-3 in the Boston Heart HDL Map Test is one of the specific subpopulations of high-density lipoprotein (HDL) particles measured to assess cardiovascular disease (CVD) risk. HDL particles, often referred to as "good cholesterol," play a crucial role in transporting cholesterol from the arteries to the liver for removal from the body. Among the various HDL subpopulations, α-3 HDL is particularly significant because it is involved in reverse cholesterol transport, a process that helps reduce cholesterol buildup in the arteries and thus lowers the risk of atherosclerosis and heart disease.

What does it mean if the α-3 is "Borderline"?

A borderline elevated result for the α-3 marker in the Boston Heart HDL Map Test indicates that while the levels of this HDL subpopulation are higher than average, they are not significantly high enough to guarantee optimal cardiovascular protection. This means the patient may have some capacity for effective reverse cholesterol transport, which helps remove cholesterol from the arteries and transport it to the liver for excretion, but this capacity is not at its peak.

Borderline elevated α-3 levels suggest that while the risk of cardiovascular disease (CVD) is potentially lower than in individuals with low α-3 levels, it is not as low as in those with markedly high α-3 levels. This intermediate status can be due to various factors, including diet, physical activity, genetics, and overall health conditions such as obesity, diabetes, or smoking habits.

From a diagnostic perspective, a borderline elevated result serves as a warning to reassess and possibly enhance lifestyle habits and medical treatments. The causes can range from partially healthy habits that need improvement to underlying health issues that impact cholesterol metabolism. There are usually no symptoms directly associated with borderline elevated α-3 levels, but the individual may be at a slightly increased risk for CVD compared to those with higher α-3 levels.

Treatment options to improve α-3 HDL levels and overall cardiovascular health include adopting a heart-healthy diet low in saturated fats and cholesterol, increasing physical activity, losing weight if necessary, quitting smoking, and managing stress. In some cases, medications such as statins or niacin might be recommended to improve HDL functionality and overall lipid profile. Regular follow-ups and monitoring of HDL subpopulations can help adjust these interventions effectively to reduce CVD risk.