Magnesium: Biokemi, Kliniske Anvendelser og Sundhedsmæssige Fordele

Hi everyone. Okay, so um as Roxy mentioned,  so today's seminar or webinar is called   magnesium mastery from biochemistry to clinical  applications. Um so a little bit about myself.   I have my bachelor's in biology, my masters  in occupational therapy. So I've worked in  

standard health care for about 20 years um  as an OT. I primarily work with adults. Um   I also have my master's in nutrition. I'm the  founder and owner of Longev Longevity Maven,   which is a nutrition and wellness um program  here in United States. So I'm in Arizona,  

so it's in a remote and local program. And then  I'm a clinical support specialist at Designs for   Health. Um so I primarily um work in research and  then I also uh work with practitioners when they   order a spotlight test. So either genomics or the  GI spotlight or the metabolomics they can schedule  

a consult and we'll go over their results and  the recommendations. Okay. So moving right into   the actual magnesium content. So going back to the  biochemistry of magnesium um magnesium as an earth   element is found in a neutral form. So that means  it has 12 protons, 12 neutrons that's inside the  

atom and then 12 electrons which are usually found  in the electron cloud or the electron shells. Um   there's something in biochemistry known as the oct  octet rule. And basically that means that atoms   are most stable when they have eight electrons  in their outermost shell or the veence shell. So  

if we look over here at this anatomical anatomic  structure of magnesium, we see that there's two   um electrons in the first shell, eight in  the next shell. So that's 10. And then that   leaves two left over for the outer shell. So in  order to satisfy this octet rule in the body,  

magnesium is going to readily lose those outer two  electrons. And that's what gives magnesium as this   plus two charge. So it it's a dvalent K cation.  It has a plus2 charge. And this is pretty much how   you're going to see magnesium in the body. It's  this plus two charge that allows magnium magnesium  

to bind uh to negatively charged molecules. It  competes with other dial cations ions and it's   also going to dictate how it regulates electrical  signaling and works as an enzyatic catalyst. The other property of magnesium is um something  called the hydration shell. So this doesn't  

just pertain to magnesium. It pertains to all  ions. So these positive and negative charged   ions are going to attract water. Water is  known as a dipole molecule. So it has a   partial negative charge around the oxygen  and then a partial positive charge around  

the hydrogen. So for magnesium, it's going  to attract the partial negative charge of   water molecules. So these oxygens and they  form what's called a hydration shell. What's   unique about magnesium is that it actually  has two layers to its hydration shell. So,  

it binds much more tightly to water  than calcium, potassium, and sodium. So,   this is critical. It's going to dictate how  it can move through cell membranes, but also   how it interacts with other negatively charged  molecules such as ATP, DNA, and cell membranes.

Okay. So magnesium as a dvalent cation looking  at how it binds to negatively charged molecules.   So this is just one example but this is a very  relevant example across the body. So magnesium   will bind readily to phosphate groups. We know  that phosphate is negatively charged. Some key  

examples are ATP. So adenosine triphosphate  the major energy currency in the body.   ATP is biologically active when it's bound  to magnesium because magnesium sort of helps   neutralize that negative charge. So anytime you  see ATP working in the body, it's almost always  

bound to magnesium. Another example is DNA and  RNA. So we know that the phosphate backbones   in DNA, they the negative charge can actually  repel one another. So magnesium binds to these   um phosphate backbones and it helps  stabilize the helical structure in DNA.  

It also supports and enables replication,  RNA replication and transcription. And then   cell membranes. So we know phospholipids are a  primary component of cell membranes. It's what's   gives cell membranes their hydrophilic or water  loving properties. So again the negative charge  

of the phosphate attracts the magnesium and  it's the magnesium binding to these phosphate   head groups which um influences cellular  membrane stability, fluidity and curvature.   So magnesium can can compete with other cations  ions. So that's going to be other positively  

charged molecules that includes things like  calcium, zinc, manganesees. Um, one of the   most common and well-known um interactions is  that calcium or I'm sorry, magnesium does work   as a functional calcium antagonist. So sometimes  called a calcium channel blocker. This is going to  

regulate muscle contractions, heart rhythms, and  vascular tone within the central nervous system.   We know that low magnesium levels can increase  calcium influx into neurons and that's going to   promote exytotoxicity. Um indirectly calcium or  magnesium can um uh regulate sodium and potassium  

levels and this is because it interacts with the  sodium potassium ATPAS pump. So this is going to   in influence um nerve conduction and muscle fire  and then other cations ions that it will it can   interact with or compete with zinc manganesees  and then toxic metals. So in terms of toxic metals  

these are positively charged molecules many of  them are. So leads two plus charge cadmium's two   plus charge aluminum is a 3 plus charge. So  toxic metals can compete with magnesium for   absorption into the from the GI tract. So having  adequate magnesium intake in the diet can prevent  

absorption of these toxic metals. Similarly,  toxic metals are known to replace both calcium and   magnesium in bone structures. So hydroxy appetite.  So magnesium sufficiency can help actually   preserve healthy bone composition and reduce metal  storage in bone. And then enzyme protection. So  

similarly toxic metals can displace magnesium from  the many enzymes that it works at the active site.   So adequate magnesium can protect um these enzyme  activities and biochemical pathways from these   toxic metal metals displacing magnesium. And then  magnesium is a co-actor. So something interesting  

that I found in my research and prep for this web  webinar is that many or current enzyme databases   actually see that there's over 600 enzymes that  require magnesium as a co-actor. So we do see that   300 number, but there's actually current databases  are listing over 600 enzymes that require  

magnesium as a co-actor. On top of that, there's  an additional 200 that require magnesium as an   activator, which basically means the substrate  that goes down that pathway requires magnesium   in order to be activated. So just some examples  again, these are just very few kynases which are  

very prevalent in energy pathways. Creatine kynise  is an example. Many of the uh glycolytic enzymes   are kynases. Uh various nucleic acid enzymes  so polymerases to topo isomeases, helilicases,   all of these are involved in DNA synthesis,  replication and repair. ATPASes and phosphotases  

are just another example of where magnesium  serves as a primary co-actor. Okay. So looking   at recommended daily allowance. So the define  the how we define recommended daily allowance   is the average daily level of intake sufficient  to meet the nutri nutrient requirements of nearly  

all 97 to 98% of healthy individuals. Something to  keep in mind these are population-based guidelines   to prevent overt deficiency diseases. So things  like scurvy, things like iron deficiency, anemia,   they're not necessarily levels that are meant  to support optimal levels of health, long-term  

health, or prevent disease. Um they don't the  RDAs do not account for variability in genetics,   metabolism, lifestyle, or health status. And they  also don't account for nutrient synergy. So we   know that many micronutrients work synergistically  like B vitamins, vitamin D and calcium, vitamin  

D and K2. All of those work synergistically.  They also don't account for the antagonistic   properties of micronutrients. So like calcium  and magnesium or zinc and copper, those things   can compete for absorption in the GI tract. So,  the German Nutrition Society, from what I've seen,  

and if I if this is incorrect, please correct  me in the chat, but what I saw in my um research   was that the German Nutrition Society has an RDA  for adults of 300 to 400 milligrams per day. Very   similar to the United States. And then the Federal  Institute for Health for Risk Assessment sets a  

250 milligram per day upper limit. That's for  supplements only. Similar to the United States,   we have 350 milligrams only for supplements. So,  if you're supplementing, they're saying an upper   limit, and that's to prevent adverse reactions.  The most common adverse reaction with magnesium  

is moose stools or diarrhea. Keep in mind  that things like stress, caffeine, alcohol,   and medications often increase magnesium needs  well above the RDA. Okay, so food sources. So,   I really like this table here. I actually pulled  this directly from the National Institutes of  

Health. It kind of lists some of the higher  rich richer foods of magnesium. Um, so we have   things like nuts and seeds at the top of the list,  legumes like peanuts and soy, unprocessed grains,   green leafy vegetables, some dairy, some fish.  Um, things that can inhibit the absorption of  

um, magnesium that are found naturally or found  within foods many times, not always naturally. Uh,   fitates and oxalates. So these are anti-nutrients  innate to plant foods. Um a lot of times these   will inhibit the absorption of minerals including  magnesium. Things that we can do to rel reduce  

the phitate and oxate oxalate content in food is  soaking um sprouting foods, fermenting and even   cooking methods. So usually slow cooking methods  and low heat cooking methods can reduce the fitate   content and improve magnesium absorption without  depleting all the minerals. Um, aluminum. So,  

aluminum is huge here in the United States. We we  know we find it kind of ubiquitously in grooming   and hygiene products, cookware, aluminum foil,  baking powders, even there's been shown in in   vivo and in vitro studies that aluminum can  reduce magnesium absorption by five times,  

which is pretty significant. Um, phosphorus. So,  high alumininal concentrations of phosphates, just   like calcium, can reduce magnesium absorption.  What's significant about this is phosphoric   acid is readily found or used in um sodas and soft  drinks uh as well as some other carbonated drinks.  

Now in the healthy gut and we know a lot of people  don't have a healthy gut but in a healthy gut   uh the average magnesium absorption is  approximately 30 to 50% of dietary intake. Okay. So for this slide, I really like it because  it shows you not only magnesium absorption,  

but where micronutrients and some of the  macronutrients are absorbed along the GI   tract. For magnesium, it's highlighted in red  here. We see that it's primarily going to be   absorbed in the judum and illiam intestinal tract.  However, there is literature that shows depending  

on transit times, you can actually get absorption  of magnesium across the small intestine. So the   dad including the dadum as well as even the large  colon will have some small magnesium absorption.   There is there is a chance of that. Um the  primary mechanisms that magnesium is absorbed in  

the GI tract. So there's two main ways. Passively  through parisellular diffusion. So this is between   the epithelial cells. Um this is particularly  present when magnesium intake is high. So when   you're supplementing um active transport. So this  is going to require ATP. Uh there's the primary  

um transporters that are known to support  magnesium absorption are transient receptor   potential melisastatin 6 and seven. And then we  also know that magnesium can transport across   the bloodb brain barrier and the blood  cerebral spinal fluid barrier. However,  

the mechanisms are not fully understood. There  is some data that suggests that specific forms   of magnesium appear to be better absorbed  into the CNS and we'll talk about that later. Um factors affecting absorption. So these are just  a few but hypocchlory so low stomach acid that's a  

huge one. When we eat magnesium in our food it's  usually found in salt form or the chilated form.   Stomach acid essentially dissociates mag the  ionized magnesium from that salt or from the   protein or the chlorophyll whatever it is and that  allows magnesium to be readily absorbed in the  

small intestine. If you do not have enough stomach  acid you are going to have a hard time absorbing   not only magnesium but other minerals as well as  amino acids because you need to break those things   apart so that they can be in smaller form ionized  form and absorbed in the small intestine. Other  

things that can contribute to malabsorption, brush  border damage, so things that you find in celiacs   and inflammatory bowel disease, small intestinal  bacterial overgrowth or small intestinal fungal   overgrowth and chronic dispiosis. All of these  things can contribute to actual damage to the  

brush border um which will decrease brush border  enzymes and won't allow for absorption uh or even   like the microvilli will also atrophy. So that  can also impede with absorption. Glyphosphate. So   this is huge in the United States. Um glyosphate  chelates to minerals, not just not just magnesium,  

but it's going to chilate to minerals. So this  is also going to impair magnesium absorption. And   then drug nutrient interactions. So specifically  with magnesium, oops, I skipped a slide. Sorry   about that. Specifically with magnesium, what  we're seeing here is that are specific medications  

that can actually deplete magnesium. Diuretics,  proton pump inhibitors, especially with chronic   use, certain antibiotics, and certain chemotherapy  agents are well documented to interfere with um or   to basically contribute to magnesium deficiency.  Um other things to keep in mind is that magnesium  

can actually interfere with the absorption of  certain medications and in those scenarios,   you want to make sure that you're taking them  separately. So, usually two hours apart is   what's recommended. This includes certain  antibiotics as well as bisphosphinates.

Okay. Magnesium distribution in the body. So  total body magnesium pool for the average 150   pound adult adult or 70 kilogram adult is  approximately 24 grams. Now this can range   anywhere from 20 to 28 grams in the literature  depending on body size. Of that magnesium pool  

50 to 60% is stored in bone. So a large portion  is stored in bones. 20 to 30% is found primarily   in skeletal muscles but also in some other soft  tissues. And then less than 1% or about 1% is   found in extracellular fluids and blood. Um just  like calcium serum serum magnesium levels are  

tightly regulated. So it's going to be regulated  by the same mechanisms that regulate calcium.   That includes intestinal absorption, renal  reabsorption and excretion and then exchange   with bone. So approximately 30% of magnesium can  is exchangeable from the bone. Okay. When we're  

looking at magnesium testing, so blood chemistry  first, um there's three main ways that we people   will usually use to look at magnesium levels. So  serum magnesium is the most commonly used because   it's very easy. It's pretty costefficient.  It's but it's also very insensitive. One,  

we know that only 1% or less of magnesium levels  are found in the blood. Um, so normal serum does   not rule out deficiency. You always want to keep  that in mind. We also know that just like calcium,   it's tightly regulated. So if you start  to have drops in magnes, serum, magnesium,  

you're the body's going to pull it from the bone  in order to keep that serum level in homeostasis.   Um, something else to keep in mind, a lot  of literature has started to point to what's   called chronic latent hypomagnesmia or subclinical  chronic magnesium depletion or deficiency. This  

is considered under 0.85 millm moles per liter  and there's higher association with long-term   um disease risk or and dysfunction when you have  chronic magnesium uh deficiency. The other way   to test magnesium in the blood is red blood  cell magnesium. So, this is more reflective of  

intracellular pools, which is great. It's telling  us what's going on inside the cell. It may not   still be the best indicator of reflection of total  body pool. And then we have ionized magnesium. So,   this is also probably better than serum magnesium.  It measures the free biologically active magnesium  

pool. It's often used in critically ill patients.  And it's um something to keep in mind though   again we're only reflecting it's only reflecting  the extracellular pool. Another way to look at   magnesium um from a functional medicine standpoint  is by looking at organic acid testing. So organic  

acid testing is basically going to give you an  idea of micronutrient status within the cell. So   it's they're going to go through these biochemical  pathways and some of these intermediates are going   to tell what whatever is spilling into the urine  is going to tell us what's going on with these  

biochemical pathways. So for magnesium we know  that it is a primary co-actor for many glycolytic   enzymes. So in this example here what we see is  this person has fifth quintile urinary glucose   very high urinary glucose but their pyuvic acid  and lactic acid are are good. They're in the first  

and second quint out here. So, not bad. What this  tells me when I'm looking at this, something's   going on with glucose where it's not getting  converted to pyuvate efficiently. Almost always   that's related to a magnesium insufficiency if  we're not considering like a genetic uh variant.  

Similarly, many KB cycle um enzymes also require  magnesium to work sufficiently. So, that includes   many of the dehydrogenase enzymes. So if you're  deficient in magnesium, you will start to see   elevated levels, especially at these markers that  are associated with dehydrogenase enzymes such as  

isoccitric acid here, suinic acid, these can be  elevated. Now something to keep in mind though   with long-term magnesium depletion or um other  micronutrient depletions that can affect KB cycle,   long-term depletions, you'll actually see all  these markers start to be low. But for acute L  

for acute or subclinical magnesium deficiency,  that's when you'll see some of these actually   being elevated. The other marker that's really  can be helpful in terms of pinpointing whether or   not a person has magnesium deficiency is the ura  cycle markers. So arginine, citrilline, ornithine,  

we know that the ura cycle enzymes are heavily  dependent on magnesium and manganese. So when you   start to see elevated levels of these ura cycle  cycle markers or intermediates, that's telling   you that most likely the P person is deficient  in these minerals. A couple other things to keep  

in mind um when you're looking at magnesium  insufficiency. If you're treating someone for   vitamin D insufficiency and they're not responding  like you think they should, like you feel like   they should definitely their vitamin D level  should be higher by now based off of what you've  

um the interventions that you've given the person.  That also can be from a magnesium insufficiency.   So magnesium is required for the activation and  conversion of both 25 hydroxy vitamin D in the   liver and then 125 dihydroxy vitamin D in the  kidneys. So looking at is magnesium playing a  

role in the vitamin D um deficiency state. On the  same lines, it can also interfere with repletion   of potassium. So if someone's not responding to  their potassium therapy, um there's potential that   magnesium is also playing a role here. Magnesium  deficiency is going to increase potassium  

excretion by the kidneys and that's going to  contribute to refractory or resistant treatments. Okay, so looking at deficiency signs and symptoms.  So we know that again that magnesium is involved   um in over 600 enzymes. It's found pretty  much involved in every single body system.  

So symptoms can be signs and symptoms can  be widespread and very generalized. Um,   and the thing that's significant about magnesium  deficiency signs and symptoms is that they can be   present with even mild and moderate states  of magnesium insufficiency or deficiency.  

So we have neurological symptoms like  anxiety, insomnia, migraines is a big one,   headaches, neuromuscular muscle cramps and  twitching, cardiovascular palpitations,   um impaired glucose tolerance, especially when  you feel like the person is doing everything  

else right, like they have healthy lifestyle  habits in place, but they still seem like there   is like glucose intolerant. That could be from the  magnesium insufficiency. um things like brain fog,   muscle weakness, nutrient physical exam, you  might see a brittle nails, that could also  

be things like zinc and iron of course, but  magnesium could play a role in that as well. Um hormonal impacts. So when we're looking at  magnesium deficiency, so I already touched about   this a little bit, but it can impact insulin  sensitivity and glucose tolerance. So we know  

that magnesium is required for insulin receptor  phosphorilation and and glucose uptake. So it   plays a role directly. It also supports blood  for transllocation to the cell membrane. Human   studies have shown that magnesium repletion  can improve insulin sensitivity in the PCOS  

and metabolic syndrome patient. Um and then  terms of thyroid function. So we also know that   magnesium serves as a co-actor for many thyroid  hormone synthesis enzymes as well as conversion   enzymes. So specifically the Diioinase enzymes.  So this can lead to impairments with T4 to T3  

conversion. And then sex hormones. Magnesium  optimizes androgen receptor binding. So it's   going to enhance testosterone bioactivity.  And then it also supports many steroidogenesis   uh pathways the cholesterol and steroid hormone  enzymes because it serves as a co-actor.

Okay. Looking at supplementation. So the primary  forms just like food you're going to find   magnesium in two primary forms um in supplements.  So one is inorganic salts like magnesium oxide   chloride sulfate. In general, the literature shows  that there's variable variable absorption of these  

when taken orally. Um, and they have higher GI  side effects. Chelated forms like glycinate,   citrate, malate, torrenate, these generally  speaking have better absorption and fewer laxative   effects. Um, so these are generally preferred  for most practitioners unless you're specifically  

targeting constipation or bowel regularity. Okay,  so these next two slides are just two tables here   um that give you some examples of the most  common magnesium forms that we can find in   supplementations. So we see like magnesium  bislycinate. It kind of tells you in the  

name what it's chelated to. It's chelated to the  amino acid glycine. Many practitioners like this   because glycine is a conditionally essential  amino acid. So it can serve as another way of   getting additional glycine needed. Um it also  we know that there's independent literature  

that supports glycine use for things like  sleep and relaxation. Um magnesium malate   is another example. So malate is a citric site um  citric acid cycle intermediate. So a lot of times   you will see this form preferentially used for  things that where people need that extra energy  

support or maybe they have some mitochondrial  dysfunction. So muscle recovery, chronic fatigue,   fibromyalgia I think actually are some of the  Designs for Health um cardiovascular protocols   use a form of magnesium malate. Um when we come  to this next slide here for the continuing on we  

see that magnesium acetal torate and magnesium  elaminate these have um some literature that may   suggest that they cross the bloodb brain barrier  more effectively. So they a lot of times these   are marketed as supporting cognitive health,  migraines, those kind of things. The acetal  

group here for the torate. So if you think of  like acetal lcarnitine or an acetylcysteine,   those also are supposed to be better in terms of  crossing the bloodb brain barrier. So that acetal   group really does seem to support um the movement  of whatever micronutrient across the bloodb brain  

barrier. Acetto magnesium sulfate. You usually see  this. It's almost never found orally. I would say   in general you usually see this either in IVs  or um Epsom salts. So, and that's because it   primarily it has a very strong laxative effect.  And then glycerol phosphate. I feel like this is  

a newer form of magnesium. There's not a lot of  literature on it, but it's complex with glycerol   and phosphate. Glycerol phosphate is a component  of the cell membranes. We know glycerol phosphate   is also a component of um gly glycolysis. So  it's one of the intermediates. This is often  

used for energy production, bone health,  cellular hydration, and then sleep support. Okay. So some key takeaways when you're thinking  about what kind of magnesium form should I be   using. So the evidence comparing different forms  of magnesium have mixed results. And there's some  

biases, you know, that sometimes people um have  a financial take in it. there, you know, there's   there's biases there. So, you always have to kind  of look at that. It's also very hard to decide,   is there a universally superior form of magnesium?  I would say based off of what I've been told and  

also the research that I did for this webinar,  there's not. Um, and then again, that's because   so many studies have different um, uh, dosages,  duration. There's just a heterogeneity in the   designs of these studies. Um, one thing to keep in  mind that's that I've came across universally is  

that the magnesium absorption depends on baseline  status. So, our bodies are very smart. In general,   individuals who are deficient with magnesium, your  body's going to absorb more, right? That makes   sense. The people who are sufficient with their  magnesium levels, the body's going to absorb less.  

So that's the general rule that you or the general  consensus that you see not only in studies but I   think anecdotically clinically that's also true.  Um something that I did see that was interesting   um under conditions of deficiency magnesium levels  tend to decline slower in the cerebral spinal  

fluid compared to plasma and then repletion  occurs quicker in the cerebral spinal fluid   relative to plasma. So this is one reason why  many researchers hypothesize that magnesium is   very vital for brain homeostasis because of how  it's regulated in the cerebral spinal fluid. Um  

some general recommendations different tissues  may preferentially uptake certain forms of   magnesium. So using a blend of different types of  magnesium forms might be more effective for most   individuals unless you're specifically targeting  a specific body system. um divided doses. We know  

that magnesium absor is absorbed better in smaller  doses. So, taking se smaller amounts several times   a day or a couple times a day is probably going to  maximize absorption and also um decrease risk for   adverse reactions like loose stools or diarrhea.  And then adult repletion ranges typically range up  

to 750 milligrams per day of elemental magnesium  um from supplements. uh that can be exceeded   though. Some of these research studies do go up  to 1.52 grams um when they're looking at these in   clinical research. Okay, so looking at magnesium  and stress. So I pulled this directly from a 2020  

um article by Pickering at All. I really like this  because it shows you the most frequently reported   symptoms of stress. many of those um symptoms  overlap with magnesium deficiency and we're going   to look at here there's a very strong cyclical  relationship between magnesium and stress.

Okay. So there what we know based off of in  vitro studies, animal models and even in human   studies is that magn magnesium deficiency can um  exacerbate a stress response. So a person is no   longer having a normal stress response. We also  know that long-term stress or even short acute  

stress can actually cause magnesium depletion. So  the way that stress leads to magnesium depletion,   we know that catapolamines like epinephrine and  norepinephrine or adrenaline and nor adrenaline   as well as gluccocorticoid specifically cortisol  lead to a shift of intracellular magnesium more  

moving out of the cell into the extracellular  space. That's going to allow for more excretion   of magnesium in the urine. So that's going to  contribute to magnesium depletion. This is an   older study. It's in the 1980s, but it's still  very relevant and I think a powerful study,  

white at all. They gave um some healthy subjects  infusions of adrenaline. And what they saw is it   reduced their serum and magnesium levels acutely  and then one hour after that infusion was stopped.   Um and there were no signs of magnesium um going  back up or repleting even at that one hour mark.  

Um, another study showed that chronic  sleep deprivation, so one month of sleep   deprivation in healthy men resulted in  reduced red blood cell magnesium levels. Okay. And then looking at how does um magnesium  deficiency in interfere with a healthy stress  

response. So what we see in animal models,  there's HPA access dysregulation. So magnesium   deficiency contributes to higher levels of  corticotropen releasing hormone released from   the hypothalamus and adrenalcorticotropen hormone  released from the anterior pituitary compared to  

controls. So those that are magnesium deficient  have higher levels of CR and AC released from   their their brains sympathetic nervous system  um influences. So we see that in um rodent   models that there's higher norepinephrine and  adrenaline as well as higher signs of stress,  

anxiety and restlessness in magnesium deficient  mice compared to controls. And then in human   studies, what we see is that magnesium deficiency  is associated with higher signs of physiological   stress. So that's going to be things like C  reactive protein, subjective reports of stress,  

insomnia, anxiety, headaches, those kind of  things. U magnesium inhibit inhibits glutamate   activity by binding to the enamethyl daspartate  receptors. So this is going to impact glutamate   activity in the brain that can also impact  neurotransmitter um and mood in the brain as  

well as perceived stress. Magnesium is also  a co-actor for glutamate decarboxilates and   this allows for the conversion of glutamate into  GABA. So we see that magnesium is going to play   a primary role in maintaining that glutamate to  GABA homeostasis in the central nervous system.  

Um another way that magnesium can influence  neurotransmitters as well as overall stress   levels is magnesium serves as a primary co-actor  for tryptophan hydro hydroxilase. This is going to   um allow for conversion of tryptophan into  serotonin. So, magnesium deficiency potentially  

can contribute to low serotonin levels. We do know  that low s serotonin is associated with anxiety. Okay. So, looking at our um Designs for Health  protocols, we do have one called adrenal   dysregulation hyper protocol and this is for  someone who is showing dysregulation in their HPA  

access. Potentially they have a heightened stress  response. Um so what we have here is catakola   calm. This is going to have various nutrients that  support the adrenals as well as the HBA access.   Some relaxation we have botanicals like lemon  balm um ashwagandha magnesium glycinate powder  

and neurocom. So the magnesium glycinate powder  has 300 milligrams of bis glycinate a patented   form called tracks. And then both the catacoloc  column and neuroccomm have diag I'm sorry die   magnesium malate. So this is going to have 75  milligrams of both in each of these. So a total  

of 450 milligrams if a person was to take this  on a daily basis of supplemental magn magnesium. Um moving on to cardiovascular health. So we  know that magnesium plays a primary role in   cardiovascular health in terms of electrical  signaling as well as blood pressure and  

endothelial health. So um as mentioned earlier  magnesium does serve as a natural calcium and   sodium agonist antagonist I'm sorry. So this is  going to help regulate cation traffic through   various channels. Um so this is going  to impact moardiocardial excitability.  

It's going to alter membrane potential. This can  impact arhythmias, tachicardia, fibrillation,   and congestive heart failure if a person's  deficient. We also know it serves as a co-actor   again for that sodium potassium ATP pump. This is  going to help maintain healthy membrane potentials  

necessary for all muscular contractions including  the heart. Um some u pre-clinical studies have   shown that hypomag magnesium deficiency  increases the dose of deoxin required for   rate control heart rate control and lower dose  lowers the dose um lowers the threshold for  

dioxin related arhythmias. Um in one human study,  this was a 2018 study, they looked at individuals   undergoing cabbage, so corne artery bypass  graft, and they gave magnesium prophylactyally,   so going into surgery. So half the people if there  were 82 patients I think in the study half of the  

um subjects were given magnesium orally via a  nasal grass tube and then the other half were   given magnesium through IV during their induction  of anesthesia. What they and then they monitored   them 48 hours post-operatively. What they found is  that both the oral magnesium and the IV magnesium  

were effective in managing post-operative  hypomagnesia and also um in preventing arhythmias. Okay. So looking at some of the mechanisms in  terms of how magnesium supports cardiovascular   health um we know that magnesium does a magnesium  deficit does stimulate angotensin 2 mediated  

eldoststerone. So that's going to impact um blood  pressure as well as thromboxing and various vasoc   constrictor prostaglandins. Um magnesium has a  ve favorable action on vascular endothelial um   function. It also modulates the release of nitric  oxide prostyc and endothelia 1 which is a potent  

vaso constrictor. Um epidemiological studies show  an inverse relationship between magnesium dietary   intake, intracellular magnesium levels and blood  pressure where the general um finding is that the   greater your magnesium intake, the lower risk  you have for high blood pressure. A couple  

protocols that we have for Designs for Health is  the congestive heart failure protocol and then we   also have the statin induced myopathy protocol.  So going back to the congestive heart failure   protocol, this one has CoQenol 200. Um it's going  to support energy production within the heart  

specifically. It also has triag supreme which has  three different forms of magnesium. This is going   to be 300 milligrams of a blend of magnesium  orate, glycerero phosphate and bis glycinate.   And then it also has omega triglycerides 1000.  The statin induced myopathy protocol again has  

CoQenol 200 because we know that CoQ10 can be  very effective for assisting with heart health   specifically in compromised states. Uh anado  EGGG so J the GG gold serves as a precursor to   um CoQ10 and can support CoQ10 levels and then it  also has magnesium malate. So again that malate is  

going to be a KB cycle intermediate. So can  indirectly support um energy production by   having that inside the magnesium form. Okay. And  then finally we're looking at magnesium and brain   health. So there's lots of other way protocols  that are involved for magnesium. I just want to  

keep that in mind. Um I was limited in terms of  which protocols to kind of talk about but we know   that there's lots of literature to support  magnesium and like osteoporosis for example   uh mental health. Uh but brain health um kind of  encompasses the mental health here. So looking at  

magnesium we again this is kind of going back  to the stress we know that magnesium inhibits   glutamate and it supports gabis. So it's going to  support that neuroexitatory neuroinhibitory state   in the brain. Um it helps maintain homeostasis by  preventing neuroexitatory or neurotoxic states.  

Magnesium also has an indirect role in brain  derived neurotropic factors. So brain derived   neurotropic factor is directly involved in neuron  neuron genesis as well as um firing and the   creation of different neur the linking between  different neurons. So this can impact memory  

learning and neuronal health. So higher levels of  cortisol can impact uh brain derived neurotropic   factor. So if you have chronically elevated  cortisol, you generally speaking, you're going   to have a decrease in brain derived neurotropic  factor. We know from earlier our discussion,  

what we talked about is that magnesium deficiency  can lead to a exaggerated cortisol response to a   to stress. So indirectly magnesium can play  a role in how much brain derived neurotropic   factor a person is synthesizing and releasing. um  higher there's a higher association of magnesium  

deficiency in neurogenerative diseases across the  board. So again this is an association. We don't   have causal factors quite yet in the literature  but there are associations. So we see magnesium   deficiency is much more prevalent in individuals  who have Alzheimer's disease, Parkinson's disease  

and even mild cognitive decline compared  to healthy um subjects. And then in one   um in terms of mental health and mood, there was  one human study which looked at 300 milligrams of   u magnesium support given daily for eight  weeks. And what they saw is this was effective  

in reducing the their depression anxiety stress  scale scores um in symptomatic adults. uh for   individuals who had higher baseline scores,  so they were more stressed, more anxious,   um they actually found that the addition of 30  milligrams of vitamin B6 to that 300 milligrams  

of magnesium support was more effective in  reducing their stress scores and that can be   because puradoxic acid or vitamin B6 does support  cellular uptake of magnesium. Okay, so looking at   our brain health supplements. So, interestingly,  when I was looking at our brain health protocol,  

we actually we do have a brain health protocol,  but it actually doesn't include magnesium,   which was surprising to me. We do have several  supplements though that are specifically meant   for mental health, um, CNS health, brain health.  Neuromag, for example, this has 145 milligrams of  

a patent form of magnesium L38. So that's going  to be the magine or magine migrol. So this is   specifically formulated for individuals who are  more prone to migraines. This is going to have   180 mill milligrams of d magnesium malate. And  then our triag supreme and triang supreme night.  

Again these are going to have the blend of three  different forms of magnesium. So 300 milligrams of   magnesium orate glycerero phosphate and bismate.  Uh the me the my triag supreme night is also going   to have um additional like botanicals that  are meant to support uh relaxation and sleep.

Okay. And then these last two slides I did  include references on the bottom of each of   the slides but I know sometimes the print can  be very small. So I just included them here as   well. So that's the end of the magnesium  um webinar. So, we'll kind of go to the  

questions now. Let's see if there anyone has any  questions. Before we start the Q&A, first of all,   I want to thank you so much for uh for doing this.  It was really super interesting. I would like to   share with everybody who is not aware of well.  This webinar was offered by Designs for Health,  

our partner. All products are available  on Welldium. Um, if you stick around,   I can show you around on the platform to see  where you can find protocols, uh, where you can,   uh, make a treatment plan and where you  can compare Designs for Health products,  

for example. Um, and yeah. Yeah, let's  go to the Q&A. I'll stop recording now.