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.

Alpha-4 High-Density Lipoprotein (α-4 HDL) is a specific subtype of HDL, commonly referred to as "good cholesterol." HDL, or High-Density Lipoprotein, is a type of protein in your blood that carries fats. The "alpha-4" designation identifies a particular size and density category within the HDL group. This α-4 HDL plays a vital role in regulating your body's cholesterol levels. It acts like a specialized waste management team, moving through your bloodstream to collect excess cholesterol from your cells and tissues, then transporting it back to your liver for disposal. This process is crucial for maintaining cell health and preventing the buildup of harmful cholesterol in your arteries.

In an Arterial Blood Gas (ABG) analysis, the term A-a O2 refers to the alveolar-arterial oxygen gradient. It measures the difference between the oxygen concentration in the alveoli of the lungs and the arterial system. Alveoli are tiny, balloon-shaped air sacs in the lungs that perform gas exchange between inhaled air and the blood.

This gradient is important because it can help to identify how well oxygen is being transferred from the lungs to the blood. A larger-than-normal gradient suggests that there may be a problem with oxygen transfer, which could be due to various reasons such as lung diseases or issues with the pulmonary circulation.

Alcohol consumption can result in elevations of the plasma Alpha-ANB/Leucine ratio. But to see this biomarker as a conclusive marker for alcoholism is not proven. The increase in the plasma Alpha-ANB/Leucine ratio does not appear to be specific for alcoholism because it was found elevated in nonalcoholic liver disease.

Alpha-Amino-N-butyric acid (α-ANB), also known as alphaaminobutyric acid, is a nonessential amino acid derived from the catabolism of methionine, threonine, and serine. α-ANB is both formed and metabolized by reactions which require vitamin B6 as a cofactor.

Alpha-Amino-N-butyric acid (α-ANB), also known as alphaaminobutyric acid, is a nonessential amino acid derived from the catabolism of methionine, threonine, and serine.

α-ANB is both formed and metabolized by reactions which require vitamin B6 as a cofactor.

Alpha-Amino-N-butyric acid (α-ANB), also known as alphaaminobutyric acid, is a nonessential amino acid derived from the catabolism of methionine, threonine, and serine. α-ANB is both formed and metabolized by reactions which require vitamin B6 as a cofactor.

Alpha-Amino-n-butyric acid (A-ANB/α-Amino-N-butyric acid) is an intermediate occurring in the catabolism of two essential amino acids, methionine, and threonine.

Alpha-aminoadipic acid (a-Aminoadipic acid) is an intermediary metabolite of lysine (primarily) and tryptophan.

Alpha-aminoadipic acid (also known as 2-aminoadipic acid) is an intermediary biomarker of lysine and tryptophan metabolism. The further metabolism of alpha-aminoadipic acid to alpha-ketoadipic acid requires vitamin B6.

Plasma alpha-aminoadipic acid is strongly associated with the risk of developing diabetes as seen in an assessment of the Framingham Heart Study data. Circulating levels were found to be elevated for many years prior to the onset of diabetes. Preclinical data shows it may also play a role in oxidation and atherosclerotic plaque formation.

Alpha-aminoadipic acid (also known as 2-aminoadipic acid) is an intermediary biomarker of lysine and tryptophan metabolism. The further metabolism of alpha-aminoadipic acid to alpha-ketoadipic acid requires vitamin B6.

Plasma alpha-aminoadipic acid is strongly associated with the risk of developing diabetes as seen in an assessment of the Framingham Heart Study data. Circulating levels were found to be elevated for many years prior to the onset of diabetes.

Preclinical data shows it may also play a role in oxidation and atherosclerotic plaque formation.

Alpha-aminoadipic acid (also known as 2-aminoadipic acid) is an intermediary biomarker of lysine and tryptophan metabolism. The further metabolism of alpha-aminoadipic acid to alpha-ketoadipic acid requires vitamin B6.

Plasma alpha-aminoadipic acid is strongly associated with the risk of developing diabetes as seen in an assessment of the Framingham Heart Study data. Circulating levels were found to be elevated for many years prior to the onset of diabetes. Preclinical data shows it may also play a role in oxidation and atherosclerotic plaque formation.

- An intermediate metabolite of lysine metabolism, produced primarily under oxidative stress (metal-catalyzed oxidation).

- In adolescents, α-aminoadipic acid was associated with adipogenesis and insulin resistance.

- Higher plasma α-aminoadipic acid was associated with a 4-fold risk of future diabetes and identified risk up to 12 years before the onset of overt disease.

- BCAAs, cystine, α-aminoadipic acid, phenylalanine, and leucine + lysine were significantly increased in obesity, T2D, and with worsening health.

Alpha-aminoadipic acid (also known as 2-aminoadipic acid) is an intermediary biomarker of lysine and tryptophan metabolism. The further metabolism of alpha-aminoadipic acid to alpha-ketoadipic acid requires vitamin B6.

Plasma alpha-aminoadipic acid is strongly associated with the risk of developing diabetes as seen in an assessment of the Framingham Heart Study data. Circulating levels were found to be elevated for many years prior to the onset of diabetes. Preclinical data shows it may also play a role in oxidation and atherosclerotic plaque formation.

Alcohol consumption can result in elevations of the plasma Alpha-ANB/Leucine ratio. But to see this biomarker as a conclusive marker for alcoholism is not proven. The increase in the plasma Alpha-ANB/Leucine ratio does not appear to be specific for alcoholism because it was found elevated in nonalcoholic liver disease.

Alpha-Hydroxybutyrate is a by-product of glutathione production. Levels of alpha-hydroxybutyrate in the urine may reflect levels of glutathione production.

a-hydroxybutyric acid (2-hydroxybuturic acid [2-HB]) is a marker that relates to oxidative stress.

a-hydroxybutyric acid is an organic acid produced from a-ketobutyrate via the enzymes lactate dehydrogenase (LDH) or a-hydroxybutyrate dehydrogenase (HBDH).

α-hydroxybutyric acid (2-hydroxybuturic acid [2-HB]) is a marker that relates to oxidative stress. 2-HB is an organic acid produced from α-ketobutyrate via the enzymes lactate dehydrogenase (LDH) or α-hydroxybutyrate dehydrogenase (HBDH). These enzymes are catalyzed by NADH. Oxidative stress creates an imbalance in NADH/NAD ratios, which leads directly to the production of 2-HB. Being that 2-HB’s precursor α-ketobutyrate is a byproduct in the glutathione (GSH) synthesis pathway, an increased demand for GSH may ultimately result in increased 2-HB. Increased oxidative stress associated with insulin resistance increases the rate of hepatic glutathione synthesis. Plasma 2-HB is highly associated with insulin resistance and may be an effective biomarker for prediabetes. A study on type 2 diabetics showed that GSH infusion restored the NADH/NAD balance and resulted in improvement of insulin sensitivity and beta cell function.