Phytohemagglutinins (PHA) Lectins bind to Mitochondria triggering a mitochondria-mediated apoptosis causing cells to age-prematurely. Symptoms of Mitochondrial Damage such as fatigue, muscle pain, shortness of breath, and abdominal pain can easily be mistaken for collagen or vascular disease, chronic fatigue syndrome, fibromyalgia, or psychosomatic illness. Mitochondrial damage is poorly diagnosed, and when symptoms do occur, they can run the range from mild, to severe, to life threatening.
Lectin Phytohemagglutinins (PHA) are produced by plants. Yes, even Organic fruit and produce. These Phytohemagglutinins firmly stick together Red Blood Cells of ALL Blood Types and White Blood Cells to form clumps. This clumping of Red Blood Cells and White Blood Cells makes passage down blood vessels and capillaries difficult resulting in hypoxia and poor immune responses.
Cell in your body require the delivery of oxygen by Red Blood Cells to Mitochondria to produce energy. This must occur for every cell in your body. Without this energy, the cells of the brain, nerves, stomach, joints, muscles, etc. cannot perform as they should. When Red Blood Cells can no longer can no longer provide oxygen for mitochondria; the cells begin aging (senescence) which triggers culling by the immune system. The immune system starts attacking the tissues of your body, indirectly because of the consumption of Phytohemagglutinin lectin fruits and produce.
Rather than using Lectin Phytohemagglutinin (PHA) for the remainder of this Post, it will be shortened to Lectins.
Lectins are carbohydrate binding proteins present in all plants, even organically grown plants. Fruits produce lectins while growing until ripe for picking. The fruit comes easily off the plant. If you have ever been around a garden. You would know they do not all ripen simultaneously. They are in varying stages of ripeness at about the same time. For the home gardener, they can go out daily to harvest the most ripe. This presents a problem for the commercial grower when harvesting a crop. Yes, even the Organic commercial grower. They cannot present produce at varying stages of ripeness to the market. They must somehow ripen the fruit so it is uniform, but we will get to that later.
Lectins make the fruit taste bad and too hard to eat while hard enough to survive shipping long distances to market. Vegetables produce lectins when the plant produces seeds. Young vegetables are sweet and taste good. Lectins make the vegetables bitter and distasteful to protect the plant while the seeds mature.
Lectins help the seed survive to maturity. Some seeds need extra protection from lectins. The softer the seed pod – the more toxic the lectins, i.e. legumes. Some seeds must survive high heat and humidity, i.e. legumes and bananas. This makes it necessary to produce lectins that resist heat and humidity.
Plants Use Lectins For Survival
Lectins have severe effects on reproductive ability, growth, and health of insects. Insects such as Apple Maggots (immature apples) or Monarch Butterfly caterpillars (milkweed or Paw Paw) consume plants and fruit that make them toxic to their predators. Plants produce toxic lectins that protect the plant and their fruit from being consumed by Insects. Thus, lectins are consequently useful as agents of insect resistance when introduced into Genetically-Modified Plants. To date, little focus has been given to the exact molecular mechanism for insecticidal activity of plant lectins by healthcare professionals.
Under normal circumstances, insects consume lectins through feeding on the plant and fruit. Therefore, the first exposure to lectins will be located in the digestive tract. Lectins bind to gut intestinal epithelial cells in insects and humans, which cause damage to intestinal epithelial cells and disruption of nutrient assimilation. After eating the plant and/or fruit, the lectin contained within are able to pass through the intestinal epithelial barrier, a whole new set of problems are created.
The cells of the body are members of a highly organized community. The number of cells in this community is tightly regulated—not simply by controlling the rate of cell division, but also by controlling the rate of cell death. If cells are no longer needed, they commit suicide by activating an intracellular death program. This process is therefore called programmed cell death, although it is more commonly called apoptosis (from a Greek word meaning “falling off,” as leaves from a tree).
Lectins cause mitochondrial transmembrane potential (MMP) collapse, cytochrome-C release, activation of caspases eventually triggering a mitochondria-mediated apoptosis. Mitochondrial DNA damage induces apoptosis in cells making up the tissues in the body causing cells to age-prematurely becoming senescent.
Caspases (cysteine-aspartic proteases, cysteine aspartases or cysteine-dependent aspartate-directed proteases) are a family of protease enzymes playing essential roles in programmed cell death (including apoptosis, pyroptosis and necroptosis) and inflammation.
Senescent cells are cleared by the Th17 immune system. Similarly, senescent cells induced during wound repair are cleared by the immune system. Th17 cells produce Th1-like cells and are self-renewed and carry on as IL-17A-secreting cells. Th17 cells are not always short-lived or age; in fact, some are a capable of persistence and functionality for a long time. Thus those consuming high amounts of lectins are constantly provoking their immune system to attack their own tissues. Inducing the onset of autoimmune conditions while never associating their diet of fresh fruit and vegetables as a contributor.
Lectins induce apoptosis in White Blood Cells (WBC) by triggering an intrinsic mitochondrial destruction and also increase ROS (Reactive Oxygen Species).
Reactions to foods containing Lectins do not need to be induced by classical antibody stimulation tested for in popular lab test results. Lectins drive distinct Th1, Th2 and Th17 immune cells to a ‘‘forbidden’’ cytokine production: Th2 cytokines responses from a Th1 immune cells, Th17 cytokine responses from Th2 immune cells and vice versa. This breakdown of the strict commitment of T cells to a distinct Th1, Th2 or Th17 reactions results in an altered immune response. The onset of autoimmune diseases first depends on a failure of self-tolerance and the appearance of “forbidden” self-reactive immune cells in the body.