Category: endothelium

The Role of Protein on Cardiovascular Disease and Associated Cardiac Events

How does protein deamination affect atherosclerotic plaque, cardiovascular health, and arterial calcification?

Protein deamination, a process where amino groups are removed from amino acids, can have several implications for cardiovascular health, particularly in the context of atherosclerotic plaque formation and arterial calcification. Here’s how these processes are interconnected:

  1. Atherosclerotic Plaque Formation:
    • Role of Amino Acids: Certain amino acids, especially those containing sulfur (like homocysteine), can influence atherosclerotic processes. Elevated levels of homocysteine, which can result from abnormal protein deamination, are associated with an increased risk of atherosclerosis.
    • Inflammatory Response: Deaminated proteins or amino acids might be seen as foreign by the body, triggering an immune and inflammatory response. This inflammation can contribute to the development of atherosclerotic plaques.
  2. Cardiovascular Health:
    • Endothelial Dysfunction: Abnormal protein deamination can lead to the production of substances that are harmful to the endothelial lining of blood vessels. This can result in endothelial dysfunction, a precursor to atherosclerosis.
    • Oxidative Stress and Inflammation: The by-products of protein deamination can contribute to oxidative stress and inflammation, which are key factors in the development of cardiovascular diseases.
  3. Arterial Calcification:
    • Calcium Deposition: Certain by-products of protein deamination can contribute to the calcification process in arteries. This calcification can make the arterial walls stiff and less elastic, increasing the risk of hypertension and other cardiovascular problems.
    • Vascular Smooth Muscle Cells: Protein deamination influences the behavior of vascular smooth muscle cells, promoting their transformation into a type that deposits calcium, thus contributing to arterial calcification.
What role do protein deamination and excess circulating phosphorus that results from deamination play in atherosclerosis?

Protein deamination and excess circulating phosphorus, both arising from metabolic processes in the body, can have significant roles in the development and progression of atherosclerosis. Here’s how these factors are interlinked:

  1. Protein Deamination:
    • Endothelial Dysfunction: Protein deamination results in the formation of various by-products, such as ammonia and keto acids. These by-products can cause endothelial dysfunction, a key factor in the initiation of atherosclerosis. Endothelial cells line the inner walls of blood vessels, and their dysfunction can lead to reduced nitric oxide availability, increased oxidative stress, and inflammatory response, all of which contribute to atherosclerotic plaque formation.
    • Inflammatory Response: The by-products of protein deamination can also trigger an immune response, leading to chronic inflammation. Inflammation is a crucial element in developing atherosclerotic plaques, contributing to their growth and instability.
  2. Excess Circulating Phosphorus:
    • Vascular Calcification: High levels of phosphorus in the blood, often a consequence of impaired kidney function or dietary factors, can lead to vascular calcification. This process involves the deposition of calcium and phosphorus in the arterial walls, making them stiffer and more prone to damage. Vascular calcification is a significant risk factor for atherosclerosis and cardiovascular diseases.
    • Oxidative Stress and Endothelial Dysfunction: Excess phosphorus can induce oxidative stress and further exacerbate endothelial dysfunction. This creates a cycle where impaired endothelial function leads to more plaque formation and arterial stiffness, escalating the progression of atherosclerosis.

The relationship between protein deamination, phosphorus levels, and atherosclerosis highlights the importance of maintaining a balanced diet and proper kidney function, as kidneys play a crucial role in regulating phosphorus levels. Individuals with chronic kidney disease are particularly at risk, as they often have elevated phosphorus levels and altered amino acid metabolism, which can accelerate the development of cardiovascular diseases, including atherosclerosis.

Therefore, in the context of cardiovascular health, it’s essential to monitor and manage factors like protein intake and phosphorus levels, especially in individuals with pre-existing health conditions that might predispose them to these metabolic imbalances.

What amino acids contain sulfur?

Sulfur-containing amino acids are primarily characterized by the presence of sulfur in their molecular structure. The most commonly known sulfur-containing amino acids are:

  1. Methionine: This is an essential amino acid, meaning that the human body cannot synthesize it, and it must be obtained from the diet. Methionine plays a critical role in many cellular processes, including the initiation of protein synthesis.
  2. Cysteine: Unlike methionine, cysteine can be synthesized in the human body, although its synthesis depends on the availability of methionine. Cysteine is important for protein structure, as it can form disulfide bonds that help maintain the three-dimensional structure of proteins.
  3. Homocysteine: This is a non-protein amino acid, typically formed as an intermediate in the metabolism of methionine and cysteine. Elevated levels of homocysteine in the blood are considered a risk factor for cardiovascular diseases.
  4. Taurine: Although not incorporated into proteins, taurine is an important sulfur-containing amino acid found in many tissues, playing a role in bile salt conjugation, eye health, cardiac function, and the development and function of skeletal muscle, the central nervous system, and the cardiovascular system.
  5. Cystine: This is a dimeric amino acid formed by the oxidation of two cysteine molecules, which are linked by a disulfide bond. Cystine is more stable than cysteine and plays a role in the structural and functional aspects of various proteins and enzymes.

What foods are highest in methionine, cysteine, homocysteine, taurine, and cystine?

Different foods are rich in various sulfur-containing amino acids like methionine, cysteine, homocysteine, taurine, and cystine. Here’s a breakdown of foods high in each of these amino acids:

  1. Methionine:
    • Animal Proteins: Chicken, turkey, beef, pork, and fish are excellent methionine sources. Eggs, particularly egg whites, are also rich in this amino acid.
    • Dairy Products: Milk, cheese, and yogurt contain good amounts of methionine.
    • Plant-Based Sources: For vegetarians and vegans, soy products (like tofu and soybeans), nuts (such as Brazil nuts and almonds), and seeds (like sesame and sunflower) are good plant-based sources.
  2. Cysteine:
    • Animal-Based Foods: Like methionine, cysteine is high in meats (chicken, pork, beef), eggs, and dairy products.
    • Plant Sources: Whole grains (like wheat germ and oatmeal), legumes (such as lentils and chickpeas), and seeds are good plant sources of cysteine.
  3. Homocysteine:
    • Homocysteine is not typically obtained directly from the diet. Instead, it is produced in the body from methionine. Therefore, foods high in methionine can indirectly contribute to homocysteine levels.
  4. Taurine:
    • Seafood and Fish: Particularly high in taurine, with shellfish (like clams, scallops, and shrimp) and fish (such as salmon and mackerel) being excellent sources.
    • Meat: Chicken and beef also contain taurine but in lower amounts compared to seafood.
    • Dairy: Some dairy products have taurine but in smaller quantities.
  5. Cystine:
    • As with cysteine, cystine is found in high-protein foods like meats, eggs, and dairy products.
    • Plant Sources: Beans, lentils, and whole grains also provide cystine, albeit in smaller amounts compared to animal sources.

What foods are highest in methionine, cysteine, homocysteine, taurine, and cystine? Please list them in descending order by volume.

  1. Methionine (from highest to lowest content):
    • Eggs (especially egg whites)
    • Fish (such as salmon, cod)
    • Chicken and turkey
    • Beef and pork
    • Dairy products (like cheese and milk)
    • Nuts and seeds (like Brazil nuts, sesame seeds)
    • Soy products (tofu, soybeans)
  2. Cysteine (from highest to lowest content):
    • Pork, beef, poultry
    • Eggs
    • Dairy products (cheese, milk)
    • Whole grains (wheat germ, oats)
    • Legumes (lentils, chickpeas)
    • Nuts and seeds
  3. Homocysteine:
    • Homocysteine is not typically found in foods. It’s a by-product of methionine metabolism in the body. Thus, foods high in methionine can influence homocysteine levels.
  4. Taurine (from highest to lowest content):
    • Shellfish (clams, scallops, shrimp)
    • Fish (mackerel, salmon)
    • Meat (chicken, beef)
    • Dairy (in smaller amounts)
  5. Cystine (from highest to lowest content):
    • Meats (beef, pork, chicken)
    • Eggs
    • Dairy products
    • Beans and lentils
    • Whole grains

What role do protein deamination and excess circulating nitrogen that results from deamination play in atherosclerosis?

Protein deamination and the resulting excess circulating nitrogen play roles in the development of atherosclerosis through several mechanisms:

  1. Protein Deamination:
    • Formation of Ammonia and Urea: Protein deamination leads to the release of ammonia, which is then converted to urea in the liver. Elevated levels of these nitrogenous compounds can have systemic effects on the body.
    • Endothelial Dysfunction: The by-products of protein deamination, including ammonia and urea, can contribute to endothelial dysfunction. The endothelium is the inner lining of blood vessels, and its dysfunction is a key early step in the development of atherosclerosis. This dysfunction can impair the regulation of vascular tone, promote inflammation, and enhance the susceptibility of blood vessels to atherosclerotic changes.
  2. Excess Circulating Nitrogen:
    • Oxidative Stress: An excess of nitrogenous compounds can contribute to oxidative stress, which is a state of imbalance between free radicals and antioxidants in the body. Oxidative stress damages cells and is a major factor in the initiation and progression of atherosclerosis.
    • Inflammation: Chronic exposure to high levels of nitrogenous waste products can induce inflammation, another critical factor in the development of atherosclerotic plaques. Inflammatory processes contribute to the progression of these plaques and their potential to cause cardiovascular events.
  3. Other Metabolic Impacts:
    • Impaired Kidney Function: Excess nitrogen compounds can strain the kidneys, which are responsible for filtering and excreting these waste products. Impaired kidney function is a risk factor for cardiovascular disease, partly because it leads to an accumulation of harmful substances in the blood, including those resulting from protein deamination.
  4. Interactions with Other Risk Factors:
    • Synergistic Effects with Other Cardiovascular Risk Factors: The effects of protein deamination and excess circulating nitrogen can be exacerbated when combined with other cardiovascular risk factors, such as hypertension, high cholesterol, smoking, and diabetes.

What is Autophagy?

To eat oneself is the plain meaning of autophagy. It is our body’s way of cleaning itself out. It is the way by which our body removes dead or degenerate cells that have lost their optimal functionality. This way the body can regenerate itself. It literally eats itself and in the process recycles the amino acids or proteins in a form of reincarnation, and it happens over and over again. Our body recycles itself because it is an efficient thing to do. It is the act of repeated incarnation. The process by which our body heals itself by tearing itself down and rebuilding with its own flesh through the process of granulation. A wound healing in the grandest sense of the word.

The human intestinal tract is an amazing ecosystem. A habitat for that which makes up much of our humanity. It is inhabited by diverse and complex colonies of synergistic micro-organisms that not only call us home but are also absolutely necessary for our overall health and wellbeing. We may be an individual in a sense but we are likely better understood as a host of a grand buffet of bacterial components spanning a diverse spectrum of individual players both commensal and pathogenic depending on the situation they find themselves in. It’s one big dinner table in there and there is a lot of diversity in its many different guests.

The lining of our intestinal tract which is also known as our intestinal epithelium interface interacts directly with this houseful of guests and acts as a barrier or first line of defense against bad players that might be interested in finding their way into our tissues. This lining of our intestinal tract has a number of mechanisms by which it protects us against micro-organisms that might want to attach themselves or even make their way into our vascular system. One of these mechanisms by which this is accomplished is mucus. A mucosal lining that has antimicrobial properties that can limit bacterial interaction with the host’s intestinal surface.

So important is this barrier our body even goes so far as to produce its own anti-microbial compounds by which to keep some of these bad players at play. One I find fascinating that our body generates on its own is lectin. A compound that is also a plant defense mechanism that we humans need to be careful of. We don’t want to be consuming too much of this compound as it is found in fresh produce as it will interfere with proper digestion, metabolism, and assimilation of nutrients. We refer to this dietary form of lectin as an anti-nutrient because it interferes with the absorption of nutrients like zinc, phosphorus, iron, and calcium. As you can see, we are not so different from the plants that live around us. We have common interests.

As you can see our intestinal lining plays a very important role in the maintenance of our overall health and wellbeing. Just another reason to be extremely diligent in the foods we choose to put in our mouth. Our intestines are not only our interface with the outside world but are also a banquet table and a battlefield. On one side is the outside world where the food we put in our mouth passes through for consumption by the trillions of micro-organisms that inhabit the passage, on the other our inside world(vascular), bathed in blood that leads directly into our liver through our portal vein for further processing and filtration before the blood that circulates through our intestinal lining enters back into general circulation.

And if everything is functioning as Mother Nature intended that whole internal environment will be continually recycled and reincarnated over and over again, day after day, week after week, month after month, and year after year, for a complete lifetime. What does our ingesting and assimilation will eventually be ingested in this continual process we call autophagy in which our extremely conservative body eats itself to rebuild itself for the betterment of life, not only within this creature we call us, but to benefit the greater outer world we call home. Mother Earth.