Patent Application
20190104758
Medicine and networked devices for preventing chronic diseases.
Western diets promote the digestions and absorptions of dietary fats attributable to arterial diseases and metabolic syndrome and sequelae. The present invention is far superior than the status quo practice of medicine for attempting to prevent and treat cardiovascular and cerebrovascular diseases, metabolic syndrome and sequelae. A plurality of groups, compounds of chemicals and almagamated chemicals, gene-editing technologies and husbandry for preventing and reducing cardiovascular and cerebrovascular diseases and metabolic syndrome by reducing the productions of the precursors of plasma lipoproteins and lipids involved in the arterial atherosclerosis process. Said groups, compounds of chemicals and almagamated chemicals for disrupting, decreasing and suppressing digestion and hydrolysis activities of enzymes, co-enzymes, catalysts, hormones, bicarbonate and digestive fluids and neural receptors by modifying the stomach and small intestinal acid-base and fluid milieus and disrupting, reducing and suppressing said activities by disrupting the hydrolysis of hydrolysis substrates, the transportation of said hydrolysis products to the absorbing epithelial cells and by digesting said enzymes, co-enzymes, catalysts and hormones. Networks of communication devices and printed information and illustration for instructing, monitoring and informing said fulfillments, performances and achievements of said chemicals and method.
Chronic diseases afflicting 10% Americans costing $2 trillions of the $3.3 trillion healthcare costs per annum. And the epic crises are escalating as people are living longer albeit still less healthy. Among chronic diseases of people, the leading cause of morbidity and mortality of people in the western nations is cardiovascular and cerebrovascular diseases and related such as, but not limited, arterial atherosclerosis such as, but not limited to, coronary atherosclerosis and cerebrovascular atherosclerosis leading to coronary heart disease such as, but not limited, ischemic heart, myocardial infarction and stroke, etc., and numerous common sequalae including morbidity and mortality and related health, morbidity and mortality and socioeconomic consequences. Despite numerous categories of expensive and life-long drugs—the statins, cholesterol absorption and inhibitors, bile acid sequestrants, nicotinic acid, fibric acid derivatives and omega 3 fatty acids—theoretically, for lipidemias, hyperlipidemias and dyslipidemias consequent to daily ingestions of high dietary fats and calories by millions of people having truncal obesity also known as central obesity. Millions are committed to life-long treatments and adverse side-effects with moderate to severe permanent sequelae. The efficacies of these treatments—like unsubstantiated information on physical activities, nutritions and supplements—are questionable. $billions per annum are expanded on snail oil and placebo and related consequences. Moreover, the prevalent methods and practices of preparing and consuming Western diets daily by billions of people—are most inducive for human gastrointestine to most efficiently digest, hydrolysis and absorb the dietary fats. If said failed, interventional procedures are utilized for said people in their best decades of life being afflicted by said chronic morbidity and mortality.
The current and growing albeit unsustainable $trillions per annum of socioeconomic, healthcare, pharmaceutical and intangible costs burdening billions of people and nations can be rapidly obliterated by the present invention. In other words, The number of individuals using said medications continued to increase.
Supporting supra are scientific facts documented herein based on the present applicant's basic and clinical researches. So, millenia of myths, false claims and believes and daily unhealthy practices by billions are heretofore revealed so that billions will be healthier and long live.
The present invention is a system and method for preventing and reducing cardiovascular and cerebrovascular diseases and metabolic syndrome by reducing and suppressing the productions and introductions of the hydrolysis products which are the precursors of the deleterious lipoproteins and lipids in the human hepatocytes and adipocytes. In present invention emphasizes the major hydrolysis substrate—the triglycerides also known as triacylglycerols in the animal fats being consumed by people—being digested and hydrolyzed into fatty acids and monoglycerides in the stomach, duodenum and jejunum by stomach, small intestinal, pancreatic and gall bladder enzymes, co-enzymes, catalysts, hormones and digestive fluids, bicarbonate, bile being aided by the neural receptors in said organs. Other products are cholesterols, lecithins and lysolecithins, etc.
The absorption of said hydrolysis products is very efficient by the absorbing epithelial cells of the duodenum and the first 100 cm of the jejunum. However, said digestions, productions and absorptions require that said biomechanism of and biochemical reactions in said digestions and hydrolysis must be precisely and accurately executed based on strict biological regulations and reactions in the normal stomach and small intestinal milieus. Based on said natural phenomena, the present invention disrupting, interfering and suppressing said biomechanism of and biochemical reactions and altering said stomach and small intestinal milieus to disrupt and suppress the productions at the source—stomach, duodenum and jejunum—thus availability of said precursors for liver and adipose tissue to synthesize and produce said lipids and lipoproteins in the relational events, diseases, disorders, morbidity and mortality described herein is schematically represented:
The hydrolysis of said dietary fats and absorption of said precursors by said absorbing epithelial cells>free fatty acids flux to the liver and adipose tissue>lipid and lipoprotein syntheses and metabolism by and flux out of the hepatocytes and adipocytes>apoB-containing triglyceride-rich VLDL production>hypertriglyceridemia>elevated hepatic VLDL synthesis>elevated hepatic LDL synthesis; elevated VLDL synthesis from simple carbohydrates>elevated hepatic LDL synthesis; elevated VLDL synthesis from simple carbohydrates>high-density cholesterol>increased HDL clearance>reduced HDL cholesterol>increased cholesterol-rich VLDLs>elevated atherogenic small dense LDL able to traverse inner arterial walls>atherosclerosis in vascular diseases>cardiovascular and cerebrovascular diseases.
The Metabolic syndrome—aging, sedentary>the hydrolysis of said dietary fats and absorption of said precursors by said absorbing epithelial cells>free fatty acids flux to the liver and central and truncal adipose tissue>increased insulin levels>promote hepatic fatty acid synthesis>pathogenesis of metabolic syndrome, obesity, central obesity also known as truncal obesity, lipodystrophy, changes in body mass index and waist-to-hip ratio>insulin resistance; diabetes; diabetes type 2>lipid and lipoprotein syntheses and metabolism by and flux out of the hepatocytes and adipocytes>dyslipidemia including hyperlipidemia and hypertriglyceridemia>hypertension>premature coronary heart disease; coronary heart disease; cardiovascular and cerebrovascular diseases.
The present invention producing and manufacturing a plurality of first, second, third, fourth and filth groups of chemicals, a plurality of compounds of said chemicals and a plurality almagamated chemicals—the latter when compounding of chemicals are not pharmaceutically feasible—for disrupting and suppressing said productions of said precursors which are said hydrolysis products comprising fatty acids, monoglycerides, cholesterols, lecithins and lysolecithins, etc. as further described supra.
Said first group of chemicals for modulating, reducing and inactivating hydrochloric acid, gastric enzymes, co-enzymes, hormones, catalysis and juice and neural receptors for generating and promoting said productions of precursors in said stomach, duodenum and jejunum. Said first group of chemicals for reducing and suppressing digestion and peptic hydrolysis of dietary fats such as, but not limited to, tributyrin which is a triglyceride naturally present in butter, dairy products and the likes. Tributyrin is an ester composed of butyric acid (a C4.0 short-chain lipid) and glycerol and is digested by gastric lipase with acid pH optimum of 5.5 in the stomach. In the small intestine, pancreatic lipase is inactive with tributyrin. Said first groups of chemicals are alkali comprising families of anions such as, but not limited to, carbonates, bicarbonates and hydroxides such as, but not limited to, cation carbonates, sodium bicarbonate, aluminum hydroxide and magnesium hydroxide. Said alkali inactivates hydrochloric acid, gastric enzymes, co-enzymes, hormones, catalysts and juice and neural receptors while conserving certain gastric enzymes such as, but not limited to, stomach pepsin—henceforth conserved stomach pepsin—for digestion in the small intestine as described infra. Calcium carbonate may be used albeit undesirable as calcium carbonate will yield calcium, for participating in and assisting pancreatic lipase in the productions of and transportation of said hydrolysis products in the small intestine. Sodium bicarbonate, aluminum hydroxide or magnesium hydroxide and compounds of same—in capsules, tablets, pills and the likes—can be ingested with meals comprising butter, cheeses and the likes composed of tributyrin. Sodium bicarbonate, aluminum hydroxide or magnesium hydroxide rendering alkali pH which disrupt and suppress digestion of tributyrin by gastric lipase.
Said first group of chemicals—represented herein by said sodium bicarbonate, aluminum hydroxide or magnesium hydroxide and the likes—rendering stomach close to or about pH 7—alkali pH. Stomach pepsin—an endopeptidase—is only active in an acid pH ranging from 1.0 to 4.0 depending on the substrates. First, said sodium bicarbonate, aluminum hydroxide and magnesium hydroxide reduce, disrupt and suppress the stomach enzymes such as, but not limited to, pepsin for digesting proteins and polypeptides into protein hydrolysates and amino acids which are some of the potent stimulators of the secretions and activations of duodenal and pancreatic enzymes, co-enzymes, hormones and catalysts, bile, bicarbonate, digestive fluid and neural receptors and the release of insulin.
Said first group of chemicals further comprises histamine H2-receptor blockers such as, but not limited to, omeprazole, lansoprazole, ranitidine, famotidine, nizatidine and cimetidine for achieving same objectives supra. Second, said conserved stomach pepsin in stomach chyme passes into the acid-pH duodenum—rendered by second group of chemicals infra—where said conserved stomach pepsin digests peptides such as, but not limited to, duodenal and pancreatic enzymes, co-enzymes, hormones and catalysts such as, but not limited to, pancreatic lipase, procolipase, colipase, cholecystokinin-pancreozymin, lecithinases, cholesterol ester hydrolase enterokinases, endopeptidases, exopeptidases, trypsinogen and trypsin.
Third, said sodium bicarbonate, aluminum hydroxide or magnesium, hydroxide and the likes—rendering chyme close to and at alkali pH to reduce and suppress the secretions and activations of duodenal and pancreatic enzymes, co-enzymes, hormones and catalysts, bile, bicarbonate, digestive fluid and neural receptors. As stated in the Claims, acidic foods, fluids, fruits and chyme, certain types of vegetable oils such as, but not limited to, oleate, protein hydrolysates, amino acids, fatty acids and water, sodium chloride and carbohydrate are potent stimulators of the secretion of secretin. Secretin stimulates the secretions of digestive fluid including bicarbonate and chloride and, furthermore, secretin stimulates the release of insulin by pancreas. Hydrochloric acid in the duodenum is the most potent stimulus of secretin release.
In addition, first exclusion of said acidic foods and fruits, acidic fluids such as, but not limited to, alcoholic and carbonated beverages, vinegars in salad dressings, fruit juices, tea and coffee and a long list of other acidic fluids being consumed by people and chyme, certain types of vegetable oils such as, but not limited to, oleate, protein hydrolysates, amino acids, fatty acids, water, sodium chloride and carbohydrate before, during and after meals will reduce and suppress said digestions and hydrolysis in the stomach and small intestine.
The approximate dosages of sodium bicarbonate are 1,000 mg-4,000 mg, aluminum hydroxide 100-400 mg and magnesium hydroxide 100-400 mg. However, said dosages can be titrated up and down in various types and quantities of meals to fulfill and achieve the goals and objectives of the present invention. Said medications in any combinations and proportions may be compounded into individual tablets, pills and capsules which are taken with meals.
Coated enteric second group of chemicals for modulating, reducing and suppressing the productions of said precursors in said small intestine, said second chemicals comprises chemicals for reducing and suppressing activities of stomach, duodenal and pancreatic enzymes, co-enzymes, catalysts, hormones and digestive fluids and neural receptors in the stomach, small intestine and brain for generating said precursors in said small intestine and the transportation and delivery of said precursors aka hydrolysis products to said absorbing epithelial cells, said chemicals for producing acid-pH duodenum and jejunum comprise:
first, ascorbic acid for producing said rendered acid-pH small intestine for suppressing the activities of said stomach, duodenal and pancreatic enzymes, co-enzymes, catalysts and hormones which are polypeptides and digestive fluids and neural receptors in the stomach,
said ascorbic acid tor producing acid pH for suppressing the emulsification by amino acids, lecithin, lysolecithin, fatty acids, monoglycerides, diglycerides, and bile acids, said ascorbic acid is coated enteric ascorbic acid being passed from stomach into the small intestine;
second, citric acid for producing acid pH for suppressing the activities of pancreatic lipase, procolipase, colipase, cholecystokinin-pancreozymin, cholesterol ester hydrolase, trypsinogen, trypsin, bile, fluid and bicarbonate,
in addition, second exclusion of amino acids, certain types of vegetable oils such as, but not limited to, oleate and corn oil, alcoholic and carbonated beverages, vinegars in salad dressings, fruit juices, tea and coffee and a long list of other acidic fluids, water which change the rates of cholecystokinin-pancreozymin release which causes the secretions of bile and pancreatic juice into the small intestine.
Citric acid for producing acid pH for suppressing the emulsification by amino acids, lecithin, lysolecithin, fatty acids, monoglycerides, diglycerides, and bile acids, said citric acid is coated enteric citric acid;
third, said citric acid for suppressing the role of calcium for hydrolysis and removing hydrolysis products into the aqueous phase, said citric acid is a chelating chemical for reducing and suppressing the activity of pancreatic lipase in said hydrolysis and said transportation of hydrolysis products at and away from said hydrolysis site so that said pancreatic lipase can remain active, said citric acid for chelating said calcium, said citric acid is a coated enteric chelating agent being passed from stomach into the small Intestine. Other organic chelating agents—oligomer, polymers and inorganic polyphosphate—are such as, but not limited to, PAA, pentasodium tripolyphosphate (STPP), ethylene diamine tetraacetic acid (EDTA), maleic acid oligomere (MAO), NTA and CMOS.
Said third group of chemicals for reducing and depriving said hydrolysis substrates for said pancreatic lipase and bile comprising coated enteric chemicals for competing for hydrolysis by pancreatic lipase and bile. Said chemicals comprise animal, plant, man-made and synthetic lipids and any combination thereof. Said third group of chemicals can be made from specific short-chain fatty acids, long-chain fatty acids, very long-chain fatty acids and glycerol moieties. Said chemicals being emulsified in the small intestine wherein said lipid-aqueous interface competing with dietary lipid-aqueous interface for pancreatic lipase at said interfaces where the pancreatic lipase is active. Because pancreatic lipase has substrate specificity—the rate of hydrolysis by pancreatic lipase is low for triglycerides with acetyl (C2) chains in the 1 position, is maximal for proprionyl (C3) and butryryl (C4), and decreases to a constant plateau for lauryl (C12) and longer chain. The animal, plant, man-made and synthetic lipids comprise short-chain fatty acids, long-chain fatty acids and very long-chain fatty acids at 1 position, 2 position and/or 3 position for producing said lipid-aqueous interface where pancreatic lipase is active but said moieties lack or have less specificity for said gastric lipase and pancreatic lipase. Furthermore, said animal, plant, man-made and synthetic lipids and any combination thereof can comprise saturated fat profile dissimilar to saturated fat profile said animal fats and unsaturated fat profile dissimilar to saturated fat profile of said animal fats. Said saturated fats such as, but not limited to, proprionic acid C3, butyric acid C4, valeric acid C5, caproic acid C6, enathic acid C7, . . . C8, . . . C9, . . . C10, . . . C11, lauric acid C12, . . . C13, myristic acid C14, . . . C15, palmatic acid C16, margaric acid C17, stearic acid C18, . . . C19, . . . C20, . . . C21, . . . C22, . . . C22, . . . C23, . . . C24, . . . C25, . . . C26, . . . C27, . . . C28, . . . C29, . . . C30, . . . C31, . . . C32, . . . C33, . . . C34, . . . C35, . . . C36, heptatriacontanoic acid C37, octatriacontanoic acid C38 and saturated fats and monosaturated fats and polyunsaturated fats in plant oils such as, but not limited to, canola oil, cashew oil, coconut oil, corn oil, cottonseed oil, olive oil, palm kernel oil, palm oil, peanut oil, rice bran oil, safflower oil, flaxseed oil, sesame oil, soya bean oil, almond oil, macadamia oil, walnut oil can be used, modified and/or re-synthesized to achieve said goals and objectives. Said fats also can be biochemically synthesized and manufactured from several-carbon substrates.
Said fourth group of chemicals for depriving said absorbing epithelial cells of said hydrolysis products comprises: First, said third group of chemicals by depriving pancreatic juice and bile of hydrolysis substrates so that less or no hydrolysis products are produced for transportation from the lipid-aqueous interface to the absorbing cells.
Second, said coated enteric chelating agents including citric acid, said citric acid for chelating said calcium, said citric acid for suppressing the role of calcium in hydrolysis and removing hydrolysis products into the aqueous phase to suppress the activity of pancreatic lipase in said hydrolysis and said transportation of hydrolysis products to said absorbing epithelial cells.
Third, a group of fatty acid-binding proteins for transesterification with said hydrolysis products—fatty acids, monoglycerides and diglycerides—in said small intestine. Said fatty acid-binding proteins (FABPs) are ligands. All FABPs have strong affinity and bind long-chain fatty acids with differences in ligand selectivity. B-FABP is highly selective for very long-chain fatty acids. L-FABP exhibits binding capacity for a broad range of fatty acids. Strong acids like said citric acid catalyzes said biochemical reaction. Thus, FABPs deprive said absorbing epithelial cells of said hydrolysis products.
Said fifth group of chemicals are coated enteric sequester for delivering the potency of said second, third and fourth groups of chemicals, compounds and almagamated for modulating, reducing and suppressing enzymes, co-enzymes, catalysts, hormones and digestive fluids and neural receptors in the stomach, small intestine and brain. One of the preferred embodiments of the present invention is Said third group of chemicals comprises aqueous- and acid-resistant, alkali-caused disintegrable sequester for isolating or encasing said second chemicals from said milieus in said stomach, said alkali-caused disintegrable sequester for exposing said second group of chemicals to said chyme, pancreatic juice and bile including bicarbonate and fluid and small intestinal enzymes, hormones and neural receptors. In other words, said coating is able to withstand stomach acids, passes intact along with and/or in said chyme from stomach into the small intestine where said coating disintegrates to release and expose said second group of chemicals to said stomach, small intestinal, pancreatic and gall bladder enzymes, co-enzymes, catalysts, hormones and digestive fluids, bicarbonate, bile and said neural receptors. Said coatings can be manufactured natural and synthetic materials. Two of many commercial coatings comprise ingredients; First, carnuba Wax, Colloidal Silicon Dioxide, Hypromellose, Methacrylic Acid Copolymer, Microcrystaliine Cellulose, Pregelatinized Starch, Propylene Glycol Simethicone, Sodium Starch Glycolate, Stearic Acid, Talc, Titanium Dioxide. Second, black iron oxide, cellulose, colloidal silicon dioxide, corn starch, hypromellose, polydextrose, polyethylene glycol, polyviny acetate phthalate, propylene glycol, shellac wax, simethicone, sidium alginate, sodium bicarbonate, stearic acid, talc, titanium dioxide, triacetin, triethyl citrate.
Firstly, individual coated enteric compounds comprising varying types and quantities of said first, second, third and fourth groups of chemicals can be produced and manufactured. Secondly, individual coated enteric almagamated first, second, third and fourth groups in varying types and quantities can be produced and manufactured. Thirdly, individual coated enteric almagamated chemical-compounds and individual coated enteric almagamated compounds-chemical can be produced and manufactured. The compatibilities of said chemicals will determine which of and all of supra will be produced and manufactured in pills, capsules, tablets and the likes for the consumers.
A variety of animal feeds for producing animal fats having less specificity and no specificity for gastric lipase and pancreatic lipase. Said feeds comprising said fat, protein and carbohydrate moieties for said animal to produce said animal fats having less specificity and no specificity for gastric lipase and pancreatic lipase. Monounsaturated fats and polyunsaturated fats in said plant oils such as, but not limited to, canola oil, cashew oil, coconut oil, corn oil, cottonseed oil, olive oil, palm kernel oil, palm oil, peanut oil, rice bran oil, safflower oil, flaxseed oil, sesame oil, soya bean oil, almond oil, macadamia oil or walnut oil and any combinations of said oils can be fed to animals to achieve said goals and objectives. Furthermore, said animal feeds comprise canola, cashew, coconut, corn, cottonseed, olive, palm kernel, palm, peanut, rice bran, safflower, flaxseed, sesame, soya bean, almond, macadamia, walnut or any plants and plant products originating said nuts and seeds and any combinations thereof can be fed to animals to achieve said goals and objectives. Consequently, said animals fats comprise numerous permutations of said short-chain fatty acids, long-chain fatty acids and very long-chain fatty acids at 1 position, 2 position and/or 3 position some of said permutations—in emulsified lipid-aqueous interface—lack or have less specificity for said pancreatic lipase. Moreover, some of hydrolysis products such as, but not limited to, monosaturated fats, polyunsaturated fats and long-chain fatty acids can significantly slow said pancreatic lipase hydrolysis and neither said fatty acids and monoglycerides are transported away from said interface nor absorbed by said absorbing epithelial cells. A case in point, in a first report, lard comprises 39% saturated fat, 45% monounsaturated fat and 11% polyunsaturated fat. In a second report, lard has a high concentration of palmitic acid—saturated fat, a 16-carbon chain—in the 2-position. Feeding a large amount of safflower seed oil to a pig resulted in an increase in the linoleic acid—a polyunsaturated omega-6 fatty acid, an 18-carbon chain—content of said lard and a decrease in the level of the other fatty acids. Beef, butter and egg yolk, for example, have high palmitic acid C16 and moderate stearic acid C18, cattle and poultry can be fed per supra to achieve supra and said goals and objectives. And fats in butter and other dairy produce can be modified to have less specificity or no specificity for gastric lipase selections of said animals for breedings to reproduce offsprings for producing animal fats having less specificity and no specificity for gastric lipase and pancreatic lipase.
By manipulating the DNA and selective breeding of animals for synthesizing hydrolysis substrates having less and no specificity for gastric lipase and pancreatic lipase, the present invention also provides a plurality of gene-editing technologies such as, but not limited to, such as, but not limited to, Crispr-Cas9 and its derivatives—for replacing segment or segments of DNA in animal hepatocytes and adipocytes with segment or segments of DNA for synthesizing triacylglycerols having less and no specificity for gastric lipase and pancreatic lipase. Because human pancreatic lipase has substrate specificity—the rate of hydrolysis by pancreatic lipase is low for triglycerides with acetyl (C2) chains in the 1 position, is maximal for proprionyl (C3) and butryryl (C4), and decreases to a constant plateau for lauryl (C12) and longer chain as stated supra. The small intestinal hydrolysis of said hydrolysis substrates and the absorption of said hydrolysis products is very efficient by the absorbing epithelial cells of the duodenum and the first 100 cm of the jejunum in human. In other words, inserted segment or segments of DNA of said animals will synthesize animal fats comprise triacylglycerols comprising numerous permutations of said short-chain fatty acids, long-chain fatty acids and very long-chain fatty acids at 1 position, 2 position and/or 3 position some of said permutations—in emulsified lipid-aqueous interface—lack or have less specificity for said pancreatic lipase.
Further to supra, among DNA-donor animals, plants, fungus and prokaryotes in the same species, related or different species such as, but not limited to, hooved animals, avian including poultry, cold-blooded including fish and crustacean, mammal and plants, applying gene-editing technologies for inserting DNA—synthesizing said desirable saturated fat profile and unsaturated fat profile in triacylglycerols of said from DNA-donor animals—into the genes of DNA-acceptor animals producing dietary fats comprising said desirable triacyl glycerols comprising said desirable saturated fat profile and unsaturated fat profile for reducing or preventing said, animal lipids from hydrolysis by gastric lipase and pancreatic, lipase and absorbed by said absorbing epithelial cells as described supra. Selections of said animals for breedings to reproduce offsprings for producing animal fats having less specificity and no specificity for gastric lipase and pancreatic lipase. Collarary, analyzing of said desirable triacyglycerols from said settings and otherwise, selective breeding of animals and selecting said animals having said desirable saturated fat profile and unsaturated fat profile will be performed to achieve the goals and objectives of the present invention.
The sciences supporting this application can be had from various biochemistry texts and journals such as Berg J. M. et al. Biochemistry 5th edit. 2002 W.H. Freeman and Co., New York.
It is to be understood that individual singular words, phrases, terms and terminologies can also imply individual plural words, phrases, terms and terminologies, respectively, whenever and wherever correct and appropriate based on facts, realities and usage in medicine and science. And that diets, meals, foods and fluids herein encompass any and all matters and fluids which are consumed by people.
Although various preferred embodiments of the present invention have been described based on chronic diseases, particularly, cardiovascular diseases—in a nutshells, chronic diseases and other diseases shared and have many casually related etiologies and biochemical and metabolic pathways and the likes—it will be appreciated by and obvious to those skilled in the sciences that adaptations, variations and derivatives of said embodiments are and will be made and achieved for people and animals without departing from the spirit and scope of the specification of the present invention.
Although various classes, types and species of substances, materials and fluids including chemicals, materials and fluids such as, but not limited, to those described herein have been described in a preferred embodiment of the present invention, it will be appreciated by and obvious to those skilled in the sciences that same, similar and related classes, types and species of substances, materials and fluids are and will be used and applied without departing from the spirit and scope of the specification of the present invention.
Although various preferred embodiments of the present invention have been essentially described for dietary fats, it will be appreciated by and obvious to those skilled in the sciences that adaptations, variations and derivatives of said embodiments are and will be made and achieved for other nutrients and lipids in human and animal foods and diets such as, but not limited to, proteins, carbohydrates, lipids—saturated, unsaturated, animal sources and vegetable sources—medications and the likes.
Although various preferred embodiments of the present invention have been described, it will be appreciated by and obvious to those skilled in the art and science that adaptations, variations and derivatives of said embodiments are and will be made and achieved for people, animals and machines and objects without departing from the spirit and scope of the specification of the present invention.
