I take these with every meal. They lessen the pain that I get from eating foods with certain B vitamins (B1 - Thiamin, B3 - Niacin, B6 - Pyridoxine)
Nature’s Plus Complete Digestive Aid Digestive Enzyme
Methylation. Some people’s bodies process vitamin B6 more effectively than others.
Soy Lecithin. Why it causes pain. Lecithin is converted into acetylcholine, a substance that transmits nerve impulses.
Description of Vitamin B6
The Structure and Function of Peripheral Nerves
The peripheral nervous system (PNS) is composed of motor, sensory, autonomic, and enteric neurons, as well as the glial cells that ensheathe their axons (Schwann cells) and cell bodies (satellite cells). Motor neurons innervate skeletal muscle fibers; autonomic (sympathetic and parasympathetic) neurons innervate and regulate the function of smooth muscle and secretory cells in a wide number of tissues. Sensory neurons innervate a variety of specialized sensory appendages (e.g., muscle spindles, Golgi tendon organs, Pacinian corpuscles, Ruffini corpuscles, hair follicles, touch domes) or terminate in anatomically unspecified nerve endings; each kind has precise patterns of synaptic connections in the central nervous system. In addition to their anatomical and physiological specifications, different kinds of neurons require different trophic factors for their development and perhaps even their maintenance.
The peripheral nerves themselves are largely comprised of myelinated and unmyelinated axons, typically grouped in fascicles, each of which is surrounded by a cellular barrier, the perineurium. Myelinated axons range from 1 to 10 microns in diameter. Alpha motor axons and a subset of sensory axons (Ia afferents) are the largest; most of the intermediate and smaller myelinated axons are sensory. Unmyelinated axons (C fibers) are smaller yet (typically less than 1 micron in diameter); these are autonomic and sensory axons, including those subserving nociception. Multiple unmyelinated axons and their associated Schwann cells comprise Remak bundles.
In the electron microscope, the most obvious structures in axons are neurofilaments and bundles of microtubules. Neurofilaments regulate the axonal caliber, and are composed of three subunits, termed heavy, medium, and light. Microtubules are composed of tubulins, and form the scaffolds for kinesins and dynactin; the molecular motors for orthograde and retrograde axonal transport, respectively. In spite of their deceptively simple appearance in fixed material, imaging reveals that living axons are highly active, with mitochondria and vesicles in seemingly incessant motion. Because the cell body is the site of most protein synthesis, axonal proteins must traffic great distances. Similarly, signals originating from the nerve terminal or axon itself must travel the entire length of the axon to reach the cell body.
Myelin is a spiral of specialized cell membrane that ensheathes axons except for small gaps - the nodes of Ranvier. The myelin sheath itself can be divided into two domains - compact and non-compact myelin - each of which contains a non-overlapping set of proteins. Compact myelin forms the bulk of the myelin sheath; non-compact myelin is found in paranodes (the lateral borders of the myelin sheath) and in Schmidt-Lanterman incisures (the funnel-shaped interruptions in the compact myelin). Compact myelin is largely comprised of lipids, including specialized lipids and proteins that play essential roles. Non-compact myelin is distinguished by tight junctions, gap junctions, and adherens junctions, between the apposed cell membrane of the myelin sheath.
The function of peripheral nerves is to conduct action potentials. In unmyelinated axons, action potentials conduct continuously, and slowly, about 1 meter/second. In myelinated axons, action potentials jump from node to node; this is called saltatory conduction and is much faster (up to 80 meters/second) than continuous conduction. Myelin sheaths facilitate saltatory conduction by reducing the capacitance of the internode, and by organizing axonal ion channels. In the nodal region, molecular interactions between Schwann cell microvilli and the nodal axolemma cluster voltage-gated Na+ channels, which are the source of depolarizing current required for saltatory conduction.
Causes and Classifications of Peripheral Neuropathy
Any disease of peripheral nerves can be called peripheral neuropathy, or simply neuropathy. There are many causes, but all of them injure axons or myelinating Schwann cells. Clinically, this dichotomy is reflected in the common usage of the terms "axonal" or "demyelinating" as adjectives to characterize an individual patient's peripheral neuropathy. This dichotomy has its roots in the cellular and molecular biology of axons; the very specializations that make them unique make them vulnerable to diseases. In addition to the issue of whether they are axonal or demyelinating, neuropathies can be classified according to whether they are inherited or acquired, or part of a syndrome...
Disease Mechanisms: Axonal Neuropathies
In many neuropathies, the clinical features tend to have a distal predilection, both in terms of first appearance and in ultimate severity. This suggests that axonal length is a factor in determining which neural elements are at risk. But distal distribution does not mean that the defect necessarily lies in the axon; it could just as well represent a primary neuron cell body abnormality. For instance, large doses of pyridoxine (vitamin B6) promptly kill large primary sensory neurons, whereas smaller doses cause only subtle shrinkage of these neurons and indolent, distal axonal degeneration. Thus, a modest neuronal abnormality may result in distal axonopathy, but a more severe insult of the same type may cause the neuron itself to degenerate as the primary event.
The nervous system is divided into two parts: the central nervous system, which consists of the brain and spinal cord, and the peripheral nervous system, which consists of cranial and spinal nerves along with their associated ganglia. While the peripheral nervous system has an intrinsic ability for repair and regeneration, the central nervous system is, for the most part, incapable of self-repair and regeneration. There is currently no treatment for recovering human nerve function after injury to the central nervous system. In addition, multiple attempts at nerve re-growth across the PNS-CNS transition have not been successful. There is simply not enough knowledge about regeneration in the central nervous system. Although the peripheral nervous system has the capability for regeneration, much research still needs to be done to optimize the environment for maximum regrowth potential.
Peripheral nervous system regeneration
Neuroregeneration in the PNS occurs to a significant degree. Axonal sprouts form at the proximal stump and grow until they enter the distal stump. The growth of the sprouts are governed by chemotactic factors secreted from Schwann cells.
Injury to the peripheral nervous system immediately elicits the migration of phagocytic cells, Schwann cells, and macrophages to the lesion site in order to clear away debris such as damaged tissue. When a nerve axon is severed, the end still attached to the cell body is labeled the proximal segment, while the other end is called the distal segment. After injury, the proximal end swells and experiences some retrograde degeneration, but once the debris is cleared, it begins to sprout axons and the presence of growth cones can be detected. The proximal axons are able to regrow as long as the cell body is intact, and they have made contact with the neurolemmocytes in the endoneurial channel. Human axon growth rates can reach 2 mm/day in small nerves and 5 mm/day in large nerves. The distal segment, however, experiences Wallerian degeneration within hours of the injury; the axons and myelin degenerate, but the endoneurium remains. In the later stages of regeneration the remaining endoneurial tube directs axon growth back to the correct targets. During Wallerian degeneration, Schwann cells grow in ordered columns along the endoneurial tube, creating a band of Bungner (boB) that protects and preserves the endoneurial channel. Also, macrophages and Schwann cells release neurotrophic factors that enhance re-growth.
Vitamin B6 (also known as pyridoxine) became “front page news” when it was discovered that, in megadoses, it causes such serious nerve damage and difficulty in walking that people have had to give up their jobs.
This has good diagrams and explanations of neuropathy and why we have numbness and pain. I especially related to this line "The sad fact is that after a while this misfiring of the nerves can get so bad that people are unable to walk or pick things up and can get to a point where they would rather have a limb amputated then continue with this nerve pain."
However, this article is not about B6 Toxicity. It suggests that people with nerve pain take B6! Let's none of us do that!
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