important blood test

 

Dr SHRADDHEY KATIYAR

@Wegiveyouhealt1

·

16h

BLOOD TESTS YOU CAN'T IGNORE AFTER 40 AS A MAN : Total serum Testosterone SHBG Free testosterone Homocysteine Extended Lipid Profile HBA1C Homa IR Serum Prolactin.

by useless conversations, one’s lifespan is destroyed

व्यर्थसंलपनेनायुर्नाशः कार्यो न शोभनैः ।

by useless conversations, one’s lifespan is destroyed; one shouldn’t engage in inauspicious actions. mudgala purāṇa, १२.२० how to know what act to do in a situation? śukra nīti says he who doesn’t read multiple śāstras can’t know so.

 https://x.com/ganapatyarya/status/2060510212747092159/photo/1

5 basic laws to great health.

5 basic laws to great health.

dont overload stomach, intestines and liver.

deep clean nose, teeth and intestines.

sleep before 10pm.

exposure to sun light 30 mins in morning.

keep clam and move around.

itna koi karega to 80 se 85 jayega aaram se 

and wont see doctors face even once.

please note that 

1. hard exercise is not mentioned.

2. cholesterol etc is pure bs for me.

Klotho, CKD, Phosphication, Stones, Inositol etc

https://x.com/photobiogenesis/status/1811149241202405625Bryce Hanna

@photobiogenesis

"Calcification" is a misnomer, it should be called "phosphication" or another term that highlights the process's primary dependence of phosphate rather than calcium

Calcium crystals in bone, teeth, and soft tissue are all calcium PHOSPHATE crystals

Allow me to explain, It's difficult or impossible to become "deficient" in circulating calcium because of the large reservoir that exists in bone. When calcium intake is low, hormones like parathyroid hormone (PTH) are elevated which increase breakdown of bone to release calcium.

PTH also elevates phosphate in the bloodstream, this occurs because calcium and phosphate are both released from bone, so while PTH promotes phosphate excretion it's still linked to phosphate accumulation when dietary Calcium:Phosphate ratio is off

Klotho is an important factor in aging, increasing it significantly improves longevity in rodents. While it's often conceptualized as a big-picture protein with many actions, at its heart is the simple action of decoupling calcium and phosphate metabolism. Klotho simultaneously activates channels that recycle calcium while blocking phosphate recycling, It's also a coactivator for the fibroblast growth factor (FGF) receptor family, which have various protective effects and include factors like FGF21 and FGF23

Klotho is stimulated by various factors: - exercise - sun exposure - caloric restriction - omega-3 fats - eating fructose/sugars - various polyphenol-rich foods - medicinal mushrooms - brown adipose tissue (cold adaptation and thermogenesis) - melatonin, testosterone, and T3 - nutrients like zinc and vitamin E

There are two subsets of Klotho: alpha-Klotho regulates calcium phosphate balance primarily, it drives the increase in FGF23 which is responsible for a protective increase in phosphate excretion beta-Klotho regulates energy intake, food preference, and metabolic rate by coupling with the liver hormone FGF21 which is normally responsible for the anti-aging effects of caloric restriction and methionine restriction

There's a clear axis of pro-fibrosis vs anti-fibrosis factors, and phosphication is the center of this process. Parathyroid hormone, hyperphosphatemia, and catabolic hormones like cortisol and prolactin (stimulated by PTH), all increase pro-fibrotic factors like TGF-beta

Phosphate plays an essential role in metabolism in the form of ATP Acetyl-phosphate or pyrophosphate may have served as ancient precursors to modern ATP in early life. Excess phosphate is directly toxic to cells and triggers inflammation, oxidative stress, and cancer formation.

Calcium's great benefit to early life may have been its ability to precipitate into insoluble crystals with phosphate. This allows both calcium and phosphate, which act as stress signals in excess, to be stored safely within the organism Over time this developed into bone

Calcification is dependent on phosphate, and since calcium reserves will always be present we can even argue it's caused by phosphate Low dietary calcium is what triggers the release of the stress hormone PTH High dietary phosphate blocks calcium sensing receptors and elevates PTH even in the presence of adequate dietary calcium.

he inverse of this is the anti-phosphication and anti-fibrosis factors

These include FGF23 and Klotho, as well as FGF21, both Klotho and the FGFs need to be present as they act on the same receptor

More dietary calcium is anti-phosphication as it drives phosphate into bone by stimulating calcitonin release and lowers PTH

Modern diets promote fibrosis and calcification through:

- hidden phosphate additives in processed foods

- phosphate pesticide use

- high bean/grain intake which are high in phosphate

- low dairy and leafy green intake which have a favorable Ca:P ratio

- low magnesium and K2 intake, which both reverse existing calcium phosphate deposits

Factors that increase Klotho and FGF21 are highly protective

It's most important to reduce phosphate intake and eat more calcium-rich foods

Caloric restriction, sunlight, exercise, and restriction of animal protein from methionine all raise both Klotho and FGF21

It turns out that high phosphate intake decrease FGF21, but only when paired with a normal or high calorie diet

The increase from caloric restriction or methionine restriction should be enough to offset this

https://t.co/72T3aPuY9L

https://pmc.ncbi.nlm.nih.gov/articles/PMC6213303/

Impaired phosphate excretion from reduced Klotho, excess caloric intake, etc, also drives sodium retention since both sodium and phosphate share a transporter in the kidneys

FGF21 increases insulin sensitivity, and insulin resistance in general drives sodium-sensitive hypertension

There's a large body of evidence that high phosphate intake causes kidney disease, hypertension, calcification and fibrosis, heart disease, diabetes, and more

Eating a better calcium:phosphate ratio (ideally 1:1) is a great way to slow aging and prepare metabolic dysfunction

Human Obesity: Is Insufficient Calcium/Dairy Intake Part of the Problem?

https://www.tandfonline.com/doi/full/10.1080/07315724.2011.10719989

Key teaching points:

Low dietary calcium intake is a significant risk factor for overweight in adults.

Calcium/dairy supplementation may accentuate the impact of a weight-reducing program in obese low calcium consumers.

Calcium/dairy supplementation promotes fecal fat loss and fat oxidation.

Calcium/dairy supplementation favors a decrease in energy intake and a facilitation of appetite control in obese individuals during weight loss.

Phosphate and Klotho

https://pmc.ncbi.nlm.nih.gov/articles/PMC3260960/

It is concluded that phosphate retention induces complex aging-like phenotypes. Thus, maintaining normal phosphate levels with phosphate binders in patients with CKD with declining Klotho expression is expected to reduce mineral and vascular derangements.

Klotho is a putative aging suppressor gene encoding a single-pass transmembrane co-receptor that makes the fibroblast growth factor (FGF) receptor specific for FGF-23. In addition to multiple endocrine organs, Klotho is expressed in kidney distal convoluted tubules and parathyroid cells, mediating the role of FGF-23 in bone–kidney–parathyroid control of phosphate and calcium. Klotho–/– mice display premature aging and chronic kidney disease-associated mineral and bone disorder (CKD-MBD)-like phenotypes mediated by hyperphosphatemia and remediated by phosphate-lowering interventions (diets low in phosphate or vitamin D; knockouts of 1α-hydroxylase, vitamin D receptor, or NaPi cotransporter). 

Phosphate—a poison for humans?

https://www.kidney-international.org/article/S0085-2538(16)30137-5/fulltext

Maintenance of phosphate balance is essential for life, and mammals have developed a sophisticated system to regulate phosphate homeostasis over the course of evolution. However, due to the dependence of phosphate elimination on the kidney, humans with decreased kidney function are likely to be in a positive phosphate balance. Phosphate excess has been well recognized as a critical factor in the pathogenesis of mineral and bone disorders associated with chronic kidney disease, but recent investigations have also uncovered toxic effects of phosphate on the cardiovascular system and the aging process. Compelling evidence also suggests that increased fibroblastic growth factor 23 and parathyroid hormone levels in response to a positive phosphate balance contribute to adverse clinical outcomes. These insights support the current practice of managing serum phosphate in patients with advanced chronic kidney disease, although definitive evidence of these effects is lacking. Given the potential toxicity of excess phosphate, the general population may also be viewed as a target for phosphate management. However, the widespread implementation of dietary phosphate intervention in the general population may not be warranted due to the limited impact of increased phosphate intake on mineral metabolism and clinical outcomes. Nonetheless, the increasing incidence of kidney disease or injury in our aging society emphasizes the potential importance of this issue. Further work is needed to more completely characterize phosphate toxicity and to establish the optimal therapeutic strategy for managing phosphate in patients with chronic kidney disease and in the general population.

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Much of the phosphate in beans and seeds is in the form of inositol phosphates like IP6 which help reduce phosphate intake. Phosphate additives in processed foods are in the form of soluble phosphate salts. Inositol may be protective as well through its ability to form IP6 and bind both phosphate and excess iron in the body. Iron and phosphate clearance may explain some of IP6's anti-cancer effects

Corpora arenacea or "brain sand" is further evidence that it's phosphication not calcification These are mineral deposits that form in the pineal and various parts of the brain, they're associated with neurodegeneration and aging They're composed of a combination of calcium phosphate, magnesium phosphate, ammonium phosphate, and some calcite. The overarching common theme is the inclusion of phosphate

7 Major Functions of Stomach Acid​

 7 Major Functions of Stomach Acid​

1. Sterilizes the Food: Whenever we consume food, bacteria and other microorganisms come in with the food (even if it was cooked or pasteurized). The stomach acid helps to neutralize the bad invaders we don’t want in our system (1, 2).
2. Protein Digestion: Stomach acid is necessary to begin the process of breaking down protein. Have you ever marinated meat in vinegar? Vinegar is not nearly as acidic as what your stomach acid should be, yet, over time it degrades the meat. This is what your stomach acid should be doing in a much quicker fashion.
3. Activating Pepsin: Pepsin is a proteolytic enzyme that is necessary for our body to effectively metabolize protein. Stomach acid activates pepsin from its inactive form called pepsinogen.
4. Activating Intrinsic Factor: Stomach acid helps to activate intrinsic factor which is a glycoprotein produced in the stomach that is necessary for vitamin B12 absorption.
5. Stimulating the Delivery of Bile and Enzymes: Stomach acid helps to stimulate the release of bile from the liver and gall bladder and digestive enzymes from the pancreas.
6. Closing the Esophageal Sphincter: Stomach acid is an important trigger for the contraction of the esophageal sphincter (just above the stomach) to protect the soft, delicate tissue of the esophagus from the harsh acids in the stomach.
7. Opening the Pyloric Sphincter: Stomach acid helps to active the pyloric sphincter which allows food to move from the stomach to the small intestine.

10 Ways to Improve Stomach Acid Levels: ​

1. Use Liquid Nutrition Throughout the Day: You should make at least half of your meals in a liquid form such as a protein shake or green smoothie. Protein shakes are pre-metabolized and very easy to digest and do not depend upon HCL production. If you have low HCL it is wise to have 1-2 protein shakes each day to enhance amino acid absorption and reduce stress on the GI system. This is very important to improve stomach acid levels.
2. Use Ginger: Ginger is one of the best things for improving digestive juices. Ginger is part of a group of herbs called carminatives along with peppermint, anise, cardamom, coriander, etc. I recommend drinking 2-3 cups of ginger tea each day, you can put ginger essential oil in water (2-3 drops in 8oz of water), juice a ½ inch of fresh ginger root in a green juice each day and use ground ginger on your foods. You can also consume fermented ginger which is common in Asian dishes such as kimchi.
3. Super Hydrate Outside of Meal Times: I am a HUGE advocate of optimal hydration and it is especially important if you have low stomach acid. Good hydration will help activate bowel motility and push contents through the digestive system which will reduce microbial fermentation and toxicity in the body.
4. Drink Very Little With Meat Containing Meals: Anytime you are going to have meat or any sort of heavier food (not a smoothie or a veggie salad), you should cut off drinking water at least 30 minutes before the meal apart from perhaps 2oz for taking a supplement. This will reduce any potential dilution of the gastric juices and allow for better digestion.
5. Hold Off On Water After a Meal: To allow for optimal digestion, I recommend abstaining from water or liquids until at least 30 minutes after a meal. This allows for proper stomach acid activity, sterilization, protein metabolism, etc.
6. Use Lemon and Apple Cider Vinegar: Squeezing fresh lemon or using lemon juice or apple cider vinegar on your meat and veggies helps to pre-metabolize the food. This allows for better digestion and nutrient absorption. You can either marinate foods in a lemon or ACV base or just add them as a dressing right before you consume them.
7. Eat Protein Foods at the Beginning of the Meal: The stomach will begin churning out its stomach acid when you begin eating, especially when you are consuming protein. It is very common for people to eat a salad before their protein dish, but this doesn’t work well for your HCL production. It is a much better idea to eat your protein with the salad or veggies.
8. Use Fermented Veggies: Fermented foods such as sauerkraut, kimchi, pickles, pickled ginger, etc. all contain organic acids, enzymes and probiotics which help to improve digestive juice secretions. I recommend using one of these with all of your heavier meals and especially any meal with protein.
9. Use Fermented Drinks: Fermented drinks such as ACV, coconut water kefir and lemon water (not fermented) contain organic acids that have an anti-microbial effect. So these help to reduce the bacterial load, especially the bacteria in the stomach such as H Pylori. Keeping H Pylori levels down is important for the body to be able to produce enough stomach acid.
10. Eat Your Largest Meal When You Are Most Relaxed: In order to produce adequate stomach acid, your body needs to activate the parasympathetic nervous system. If you are busy and on the go, you will be in fight or flight sympathetic mode. If you struggle with low stomach acid, this is not going to allow you to produce anywhere near enough. Relaxing before the meal is key to improve stomach acid production.