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We have said that animals obtain chemical energy from the fooda€”carbohydrates, fats, and proteinsa€”they eat through reactions defined collectively as catabolism.
In stage II, these monomer units (or building blocks) are further broken down through different reaction pathways, one of which produces ATP, to form a common end product that can then be used in stage III to produce even more ATP.
Carbohydrate digestion begins in the mouth (Figure 20.5 "The Principal Events and Sites of Carbohydrate Digestion"), where salivary I±-amylase attacks the I±-glycosidic linkages in starch, the main carbohydrate ingested by humans. Protein digestion begins in the stomach (Figure 20.6 "The Principal Events and Sites of Protein Digestion"), where the action of gastric juice hydrolyzes about 10% of the peptide bonds. The pain of a gastric ulcer is at least partially due to irritation of the ulcerated tissue by acidic gastric juice. Aminopeptidases in the intestinal juice remove amino acids from the N-terminal end of peptides and proteins possessing a free amino group.
This diagram illustrates where in a peptide the different peptidases we have discussed would catalyze hydrolysis the peptide bonds.
Lipid digestion begins in the upper portion of the small intestine (Figure 20.9 "The Principal Events and Sites of Lipid (Primarily Triglyceride) Digestion").
The monoglycerides and fatty acids cross the intestinal lining into the bloodstream, where they are resynthesized into triglycerides and transported as lipoprotein complexes known as chylomicrons. The further metabolism of monosaccharides, fatty acids, and amino acids released in stage I of catabolism occurs in stages II and III of catabolism.
In what section of the digestive tract does most of the carbohydrate, lipid, and protein digestion take place? Aminopeptidase catalyzes the hydrolysis of amino acids from the N-terminal end of a protein, while carboxypeptidase catalyzes the hydrolysis of amino acids from the C-terminal end of a protein. During digestion, carbohydrates are broken down into monosaccharides, proteins are broken down into amino acids, and triglycerides are broken down into glycerol and fatty acids. Using chemical equations, describe the chemical changes that triglycerides undergo during digestion.
What are the expected products from the enzymatic action of chymotrypsin on each amino acid segment?
What are the expected products from the enzymatic action of trypsin on each amino acid segment?
Chymotrypsin is found in the small intestine and catalyzes the hydrolysis of peptide bonds following aromatic amino acids. Pepsin is found in the stomach and catalyzes the hydrolysis of peptide bonds, primarily those that occur after aromatic amino acids.
Bile salts aid in digestion by dispersing lipids throughout the aqueous solution in the small intestine. Emulsification is important because lipids are not soluble in water; it breaks lipids up into smaller particles that can be more readily hydrolyzed by lipases. Action: hydrolysis of ester bonds between the glycerol molecules and the fatty acid chains. The lacteals (green) that receive the lipoproteins before transporting them to the circulatory system. On Wednesday a new paper reported that higher levels of long-chain omega-3 fats (EPA, DPA, and DHA) in blood are associated with a 43% increased risk of prostate cancer and a 71% increased risk of aggressive prostate cancer. In our book and on this blog, we’ve already discussed two mechanisms linking excessive omega-3 intake to cancer risk. Peroxidation of PUFA generates highly toxic compounds, such as aldehydes, which mutate DNA and turn proteins into advanced lipoxidation end products (ALEs). Second, oxidation products of DHA promote angiogenesis – the creation of new blood vessels to feed tumors.
This is a very different biomarker than the Omega-3 Index of William Harris, which looks at the omega-3 phospholipids in red blood cell membranes.
The study measured plasma phospholipid omega-3s in a group of people, then followed them for 6 years or so to see who developed cancer. The trial asked its participants not to take supplements, and it looks like they drew a study population whose fish intake was much lower than that of Framingham, Massachusetts, residents. If dietary omega-3 intake was low in all subjects and varied only slightly among participants, how do we know that this biomarker is related in any way to dietary intake?
If high dietary intake of omega-3s caused more cancer, we would expect cultures that consume lots of fish oil to have higher prostate cancer rates. Although none of these studies produced a statistically significant link between omega-3 intake and cancer, incidence of cancer diagnosis or death was increased in every one of the clinical trials except the GISSI-Heart Failure study and perhaps the Origin study. UPDATE: Vladimir Heiskanen points me to an interesting paper in which the effect of dietary fatty acids on cancer metastasis was examined. At 3 weeks after tumor transplantation, the fish oil diet and the safflower oil diet had induced, respectively, 10- and 4-fold more metastases (number) and over 1000- and 500-fold more metastases (size) than were found in the livers of rats on the low-fat diet. Minimize omega-6 intake so that omega-6 and omega-3 balance is achieved at the lowest possible intake of polyunsaturated fats.
When Amit and I first tried Paleo we had some minor setbacks, but our experience improved wonderfully on the Perfect Health Diet version of Paleo so we are grateful for the Jaminets’ wonderful book and website. I’m a practicing optometrist and recommend that all my patients regardless of age or health (except those on blood thinners or a week before surgery) eat about a pound of oily fish per week (about 4-5 servings) like wild salmon, sardines, and sablefish (black cod). Help with brain and mental issues such as ADHD, autism spectrum disorders, anxiety, depression (including prenatal and postpartum), mood, cognition, Huntington’s disease, bipolar, schizophrenia, etc. Improve cardiovascular health in aspects such as blood pressure, circulation, triglycerides, VLDL, heart attacks, and stroke. The long-chain omega 3s EPA (Eicosapentaenoic acid) and DHA (Docasahexaenoic acid) are especially important. The body can convert some ALA (alpha linolenic acid) found in plants such as flax and chia into EPA and DHA, but this conversion is often poor – as low as 0.05-15% in healthy humans and worse in older people and those with some medical conditions! I cannot recommend flaxseed also for women due to estrogenic effects that could negatively affect hormonal conditions like PCOS, endometriosis, fibroids, or any reproductive cancers.
There are so many benefits to Bengali Fish Curry, and probably more will be discovered in time – that is why I recommend it! 2.      Second, the $64,000 question: Is there evidence that high levels of dietary DHA promotes diseases of pathological angiogenesis? The papers discussed in Friday’s post about a major angiogenesis pathway stimulated by oxidized DHA (Omega-3s, Angiogenesis and Cancer: Part II, April 29, 2011) may not seem important to many readers.
A tumor is, in the words of Hal Dvorak, “a wound that never heals.” [1] To support growth, cancers invoke the wound healing process – especially, creation of new blood vessels, or angiogenesis. It’s been recognized for decades that an ability to block angiogenesis would effectively constitute a cure for cancer. If only the VEGF pathway is blocked (upper right), there is almost as much angiogenesis and wound healing as in a normal wound (upper left).
If these are the operative pathways in cancer also, then blocking the TLR-2 angiogenesis pathway might be the key to cancer therapy. Age-related macular degeneration, diabetic retinopathy, and retinopathy of prematurity – three common causes of blindness.
It may be that the TLR-2 pathway is key to these diseases as well, and that a treatment that inhibits this pathway can cure or improve all of these diseases. Some antibiotics, including doxycycline and minocycline, are known to exercise anti-angiogenic effects independent of the antibiotic effects.
If this pathway is important in human disease, then we should expect diseases of angiogenesis to be worsened by adding the ingredients on the left. Specifically, cancer, AMD, rosacea, and so forth should be worsened by high doses of DHA, high doses of vitamin A, and low doses of antioxidant minerals like zinc or selenium. A clever but unlikely alternative explanation was suggested by Peter at Hyperlipid: perhaps extra dietary fish oil raises testosterone levels. A unified explanation along this line would be: Finasteride raises DHA levels, and DHA lowers testosterone.
My bottom line: the Brasky study is weak evidence for anything, but it does raise a whiff of evidence that high dietary fish oil intake might encourage a transition from low-grade to high-grade cancer.
Retinyl palmitate (vitamin A) has been tested in clinical trials for its effect on cancer risk. The Carotene and Retinol Efficacy Trial (CARET) was a multicenter randomized, double-blind placebo-controlled chemoprevention trial testing whether daily supplementation with 30 mg β-carotene + 25,000 IU retinyl palmitate would reduce lung cancer risk among 18,314 heavy smokers, former heavy smokers and asbestos-exposed workers. As a proportion of the total prostate cancer cases, more men who were randomized to the active arm developed high-grade prostate cancer (Gleason 7-10) than in the placebo arm (44.6% vs.
Interestingly, in the placebo arm taking multivitamins and other supplements reduced cancer risk. Men with higher retinol concentrations at baseline were more likely to develop prostate cancer (quintile 5 vs.
Carotenoids, which can generally be converted to vitamin A, are also associated with higher cancer risk.
Lycopene may be the most powerful carotenoid quencher of singlet oxygen,[18] being 100 times more efficient in test tube studies of singlet-oxygen quenching action than vitamin E … The absence of the beta-ionone ring structure for lycopene increases its antioxidant action…. So lycopene does not increase retinyl levels, but does act as an extraordinarily powerful antioxidant, thus reducing oxidative stress!
The evidence here is rather mixed, because with the exception of the negative effects of vitamin A, most antioxidants seem to have little effect on cancer. I’ll skip those for now, other than to note that fish oil is a well-known trigger of rosacea. This pattern would be consistent with the idea that the natural pathway used in wound healing to trigger angiogenesis – DHA oxidation and combination with retinyl protein to trigger TLR-2 pathways – is also important for cancer progression. It suggests a strategy of reduced fish oil and vitamin A consumption and increased intake of certain antioxidants (such as lycopene, zinc, selenium, or NAC) may be helpful against cancer. Given the many proven benefits of moderate amounts of fish oil, I don’t see a reason yet to alter our recommendation that healthy people should eat a pound of fish per week. On Tuesday (Omega-3 Fats, Angiogenesis, and Cancer: Part I, April 26, 2011) I introduced the issue of possible relationships between omega-3 fatty acids, their lipid peroxidation products, and diseases of angiogenesis such as cancer, and promised to discuss a possible mechanism today.
It may be well, however, to start by saying a little bit more about the Brasky paper [1] linking prostate cancer to DHA. The study measured the fraction of serum phospholipid fatty acids in various polyunsaturated and trans-fat species, not dietary intake. Denise makes the important point, however, that the connection between dietary fish oil intake and serum fatty acid profile is not simple. However, study participants were followed for 7 years, at which point their prostate cancer status was assessed. Hospital diet advice is bad: DHA was a marker at the start of the study for conscientious, educated, disciplined persons who followed health advice and ate fish oil.
Another of Denise’s assertions is that there is an “otherwise consistent train of research showing that DHA seems protective at best (and neutral at worst).” Now it is true that there are more studies showing DHA to have benefits against cancer than harm. In the comments to Tuesday’s post, eric linked to a 2005 meta-review of studies on omega-3 fats and cancer.


So the score was 4 studies finding that DHA is associated with less cancer, 1 that it is associated with more, and a boatload that it had no association. One reason an association of DHA with high-grade cancer may have been missed is that it would be detected only in large studies able to segregate cancers by grade.
If there were no other evidence linking DHA to angiogenesis, the Brasky and EPIC study associations would be interesting, but unlikely to change anyone’s mind. We haven’t sleuthed out any mechanism that could explain why DHA (but not other polyunsaturated fats) promotes rapid tumor growth. Let’s start by going back to 2003 and a paper on the role of a compound called carboxyethylpyrrole (CEP) in age-related macular degeneration (AMD). Free radical-induced oxidation of docosahexaenoate (DHA)-containing lipids generates ω-(2-carboxyethyl)pyrrole (CEP) protein adducts that are more abundant in ocular tissues from AMD than normal human donors…. Of individuals (n = 13) exhibiting both antigen and autoantibody levels above the mean for non-AMD controls, 92% had AMD. Although rare in most human tissues, DHA is present in ~80 mol % of the polyunsaturated lipids in photoreceptor outer segments (13). Oxidative damage appears to contribute to the pathogenesis of AMD (4) based on epidemiological studies showing that smoking significantly increases the risk of AMD (1, 24). The CEP is co-localized with CD68, a glycoprotein which binds to LDL and is found on macrophages, and with CD31, a membrane marker of neutrophils, macrophages, and endothelial cells. It turns out that CEP drives angiogenesis by attaching to an immune receptor, Toll-like receptor 2 (TLR2). On the lower left is a similar wound with no VEGF inhibition, but the TLR2 pathway blocked by TLR2 knockout. If you administer CEP-neutralizing antibodies to a normal wound, wound healing takes more than twice as long. Altogether our results establish a novel mechanism of angiogenesis that is independent of hypoxia-triggered VEGF expression.
DHA is oxidized to a compound called HOHA which then combines with a protein, generally a retinyl (vitamin A-derived) protein to form CEP. Cancers generate lots of CEP from DHA, and perhaps one way they do that is by generating lots of retinyl proteins. I haven’t looked much into this literature but it may speak to higher cancer risk with excessive vitamin A intake. In the case of cancer, DHA oxidation to CEP might transform miniscule, harmless cancers to high-grade, life-threatening cancers.
I question whether DHA supplementation would truly play a causative role in the absence of a *pro-oxidative environment*.
In other words, perhaps in someone eating a SAD, not exercising, under a lot of stress, etc. As I replied to Chris in the comments, low-carb Paleo dieters are not out of the woods in regard to oxidative stress. Come to the Perfect Health RetreatCome join us for a week at the beach learning how to achieve a lifetime of great health!
Buy our bookPerfect Health Diet: Regain Health and Lose Weight by Eating the Way You Were Meant to Eat is a great way to understand the dietary and nutritional practices that lead to optimal health. AOBiome Skin ProbioticsWe recommend AOBiome's AO+ Mist skin probiotics, which help convert odorous ammonia to beneficial nitrates, and microbiome-friendly cleansing products.
See the license for more details, but that basically means you can share this book as long as you credit the author (but see below), don't make money from it, and do make it available to everyone else under the same terms. However, the publisher has asked for the customary Creative Commons attribution to the original publisher, authors, title, and book URI to be removed. We can think of catabolism as occurring in three stages (Figure 20.4 "Energy Conversions"). The secretion of I±-amylase in the small intestine converts any remaining starch molecules, as well as the dextrins, to maltose.
Gastric juiceA mixture of water, inorganic ions, hydrochloric acid, and various enzymes and proteins found in the stomach.
Pancreatic juice, carried from the pancreas via the pancreatic duct, contains inactive enzymes such as trypsinogen and chymotrypsinogen. Figure 20.8 "Hydrolysis of a Peptide by Several Peptidases" illustrates the specificity of these protein-digesting enzymes. A hormone secreted in this region stimulates the gallbladder to discharge bile into the duodenum. Phospholipids and cholesteryl esters undergo similar hydrolysis in the small intestine, and their component molecules are also absorbed through the intestinal lining. Chymotrypsin catalyzes the hydrolysis of peptide bonds following aromatic amino acids, while trypsin catalyzes the hydrolysis of peptide bonds following lysine and arginine. Thus, it doesn’t measure any omega-3s in cells, only omega-3s in serum particles like LDL, HDL, and VLDL; and even in those particles it excludes omega-3 fats found in triglycerides. There we find that subjects who went on to develop prostate cancer averaged 3% more DHA and 4% more EPA+DPA+DHA in plasma phospholipids than those who didn’t develop cancer. Both of these numbers are considerably higher than the values reported by Braskey et al., even in their highest quartile.
There could be other factors – genetics, oxidative environment, omega-6 fat intake, antioxidant intake, changes in the proportions of VLDL, LDL, and HDL, to name a few – that affect this biomarker. But epidemiological studies have found that high omega-3 intakes seem to be associated with low cancer rates.
Colon carcinoma cells were injected into the portal vein (which leads from intestine to liver) of rats and 3 weeks later rats were sacrificed and their livers were examined for metastases. However, the results are consistent with the idea that fish oil is more cancer-promoting than the less peroxidizable safflower oil, perhaps because of the unique pro-angiogenic effects of DHA products.
Cardiovascular disease causes more deaths than cancer, and omega-3 fats are protective against CVD. Serum phospholipid fatty acids and prostate cancer risk: results from the prostate cancer prevention trial. Lipid peroxidation-induced DNA damage in cancer-prone inflammatory diseases: a review of published adduct types and levels in humans.
Dietary omega-3 polyunsaturated fatty acids promote colon carcinoma metastasis in rat liver. Shilpi Bhadra Mehta is a Doctor of Optometry, a Board Member of the Archaeological Institute of America, and leader of the Boston Paleo group, Living Paleo in Boston. But when he went Paleo for health reasons he fell in love with this traditional Bengali recipe, so I make it almost weekly!
Amit and I are organizers of the Boston Paleo Meetup Group, and hosted a great potluck and lecture by the Jaminets in October 2011. DHA is the most common Omega 3 in the brain and the retina – the neural part of the eye that senses light, and part of the central nervous system (CNS)! In the often blinding eye disease Retinitis Pigmentosa (RP), RP patients compared to normals had far lower DHA in blood and sperm. EPA and DHA are most abundant in oily fish and in the breast milk of women who consume fish. A component known as curcumin has been shown to help cancer, osteoarthritis, Alzheimer’s disease, pancreatitis, psoriasis, and some infections. Efficacy of Ginger for Nausea and Vomiting: A Systemic Review of Randomized Clinical Trials. Inhibitory Effects of Zingiber officinale Roscoe Derived Components on Aldose Reductase Activity in Vitro and in Vivo. Long-chain omega-3 fatty acids for indicated prevention of psychotic disorders: a randomized, placebo-controlled trial. Reducing the genetic risk of age-related macular degeneration with dietary antioxidants, zinc, and ?-3 fatty acids: the Rotterdam study.
Nutritional manipulation of primate retinas, V: effects of lutein, zeaxanthin, and n-3 fatty acids on retinal sensitivity to blue-light-induced damage. The William Li video explains why: nearly everyone gets microscopic tumors that never develop the ability to induce angiogenesis. Avastin, an anti-angiogenic drug targeting VEGF (vascular endothelial growth factor), has been estimated to extend colon cancer patient lifespan by only 6 weeks. But when both the VEGF and TLR-2 angiogenic pathways are blocked (lower right), there is no wound healing. Adipose tissue utilizes angiogenic pathways, and angiogenesis inhibition prevents the deposition of fat. But we can still get excited over possibilities to improve these diseases through diet and anti-microbial medicine.
As a result, anti-microbial medicines might help treat some diseases of pathological angiogenesis.
In fact, cancer studies have identified dozens of plant foods, from garlic to tomatoes to leeks, that possess anti-angiogenic properties. High tissue levels of DHA were associated with increased risk of high-grade prostate cancer, and the oxidized DHA angiogenesis pathway provides a mechanism for this association.
Prostate cancer is a hormone-dependent cancer and can be promoted by testosterone, just as breast cancer is promoted by estrogen. Low testosterone reduces incidence of low-grade prostate cancers but makes it much more likely they will progress to high-grade.
The intervention ended 21 months early in January, 1996 when interim analysis found evidence that the supplements increased the risk of lung cancer and total mortality in this high-risk population by 28% and 17%, respectively (10). If you wanted a good food for stopping the DHA – angiogenesis pathway, you’ve found it: tomatoes.
If oxidized DHA drives angiogenesis, then antioxidants should be preventative for these diseases. N-acetylcysteine has been shown to prevent angiogenesis and has been proposed as a likely cancer preventative, but this is as yet untested. Observational studies weakly link high DHA, high vitamin A, and low antioxidant status to diseases of angiogenesis such as cancer.
Comparison of doxycycline and minocycline in the inhibition of VEGF-induced smooth muscle cell migration. Dietary supplement use and prostate cancer risk in the Carotene and Retinol Efficacy Trial.
Serum lycopene, other serum carotenoids, and risk of prostate cancer in US Blacks and Whites. Her conclusion – “given the oxidation-prone nature of all polyunsaturated fats, a massive intake of omega-3’s – despite their brilliance in moderation – could potentially do more harm than good” – is the proper one.
This is the right parameter to measure, as fatty acid profiles can be measured precisely while dietary intakes assessed through questionnaires are notoriously unreliable.
Higher DHA intake raises phospholipid DHA levels, but lower intake of non-omega-3 fats also raises the DHA fraction.
I don’t think it affects it much, because study participants were healthy at the start of the study with no history of cancer and macronutrient intakes don’t vary a lot among the general public. Incidence of low-grade prostate cancers had no association with start-of-the-study DHA intake, but incidence of high-grade prostate cancers was strongly associated. When these people were diagnosed with low-grade cancer, they followed the dietary advice of their cancer dietitian.
But this trend is hardly consistent, and the vast majority of studies have failed to detect a relationship.


However, for lung cancer, one of the significant associations was for increased cancer risk and the other was for decreased risk (four other risk ratios were not significant for lung cancer). One is to note that there are slightly more studies showing DHA to have benefits than harm, and therefore to judge that DHA might be helpful against cancer. Most Americans eat far too much omega-6, and their omega-6 to omega-3 tissue ratio is too high, which is pro-inflammatory via the COX-2 pathway. In fact, there is a known mechanism by which DHA but not other polyunsaturated fats can promote rapid tumor growth. The CEP adduct uniquely indicates oxidative modification from DHA derivatives because CEP protein modifications cannot arise from any other common polyunsaturated fatty acid. Its abundance depends on DHA abundance, availability of retinyl proteins, and the level of oxidative stress. The abundance of DHA in photoreceptors, the high photooxidative stress in retina, and the fact that DHA is the most oxidizable fatty acid in humans (13) suggests that DHA oxidation products may have possible utility as biomarkers for AMD susceptibility. Immunized mice develop antibodies to CEP, fix complement component-3 in Bruch’s membrane, accumulate drusen below the retinal pigment epithelium during aging, show decreased a- and b-wave amplitudes in response to light, and develop lesions in the retinal pigment epithelium mimicking geographic atrophy, the blinding end-stage condition characteristic of the dry form of AMD. That leads us to a Nature paper from October 2010 [7], from the group of Tatiana Byzova at the Cleveland Clinic. Briefly, CEP has a physiological function: it is transiently elevated in wounds and recruits immune cells from bone marrow to the site of the wound. CEP is marking endothelial cells and white blood cells in angiogenic vessels, and possibly LDL.
There are two major pathways for angiogenesis: one driven by vascular endothelial growth factor (VEGF), which is dominant in conditions of hypoxia (oxygen starvation), and one by TLR2.
This confirms that angiogenesis driven specifically by CEP (and therefore by DHA oxidation) is part of healthy wound healing. The products of lipid oxidation are generated as a consequence of oxidative stress and are recognized by TLR2, possibly in a complex with TLR1 on ECs, and promote angiogenesis in vivo, thereby contributing to accelerated wound healing and tissue recovery. Retinoids, particularly retinoic acid, have critical regulatory functions and appear to modulate tumor development and progression. But it is also invoked excessively in pathological contexts – notably in cancers and age-related macular degeneration, probably also in other angiogenesis-associated diseases such as arthritis, rosacea, obesity, psoriasis, endometriosis, dementia, and multiple sclerosis. Well, we need to know the relative importance of the three ingredients on the left side of the above equation in producing angiogenesis. Oxidative stress is generated normally during metabolism, immune function – and by cancers. Moderate omega-3 consumption is especially important for those suffering from diseases of pathological angiogenesis – especially cancer. Carboxyethylpyrrole protein adducts and autoantibodies, biomarkers for age-related macular degeneration. A hapten generated from an oxidation fragment of docosahexaenoic acid is sufficient to initiate age-related macular degeneration. You may also download a PDF copy of this book (72 MB) or just this chapter (5 MB), suitable for printing or most e-readers, or a .zip file containing this book's HTML files (for use in a web browser offline). In stage I, carbohydrates, fats, and proteins are broken down into their individual monomer units: carbohydrates into simple sugars, fats into fatty acids and glycerol, and proteins into amino acids.
HCl helps to denature food proteins; that is, it unfolds the protein molecules to expose their chains to more efficient enzyme action. The amino acids that are released by protein digestion are absorbed across the intestinal wall into the circulatory system, where they can be used for protein synthesis. The principal constituents of bile are the bile salts, which emulsify large, water-insoluble lipid droplets, disrupting some of the hydrophobic interactions holding the lipid molecules together and suspending the resulting smaller globules (micelles) in the aqueous digestive medium. For instance, the Japanese eat eight times more omega-3 fatty acids than Americans and their blood levels are twice as high, yet the prostate cancer rates are only one-sixth the American rate. The rats were on three diets — low-fat, high omega-6 (safflower oil), high omega-3 (fish oil). I asked her to tell us about Indian cuisine, and she offered a discussion of Bengali Fish Curry. Bengal is part of India and Bangladesh, it is the home of Bengal tigers, but it is most famous for eating and cooking fish. About 60% of the polyunsaturated fatty acids (PUFA) in the retina are from DHA, and 40% of the brain’s PUFA is DHA. In rodent studies flaxseed affected menstrual cycle, lowered birth weight, and altered reproduction in offspring including infertility.
Thus, finasteride reduces prostate cancer incidence but increases high-grade prostate cancer incidence and overall prostate cancer mortality.
And I’m intrigued by the idea that dietary changes may have the potential to play a powerful role in recovery from diseases of angiogenesis such as cancer.
Also, phospholipids are the fats in cell membranes, and these are the ones involved in the inflammatory signaling pathways long thought to drive cancer risk. Americans vary surprisingly little from the median of about 50% carbs, 15% protein, and 35% fat – so it’s likely that the quartile with high tissue DHA levels were also high fish oil consumers. Given that the Prostate Cancer Prevention Trial and the European Prospective Investigation into Cancer and Nutrition, the 2 largest studies of blood levels of phospholipid fatty acids, reported increased risks of high-grade prostate cancer with high levels of ω-3 fatty acids, it remains a possibility that these fatty acids promote tumorigenesis.
Basically, malformed blood vessels overgrow the eye, causing retinal detachment and blindness.
We speculate that reactive oxygen and nitrogen species derived from tobacco smoke in the lungs leads to oxidative protein modifications in the blood that contribute to drusen formation and choroidal neovascularization.
Inflammatory cells are present in the region of lesions and may be actively involved in the pathology observed. These immune cells further increase oxidative stress and promote angiogenesis; CEP levels are highest at the time of peak angiogenesis. If high levels of CEP and its analogs accumulate in tissues, it may lead to excessive vascularization, e.g. If anti-oxidant minerals like zinc, copper, and selenium and vitamins like vitamin C are deficient, then oxidative stress can be very high on a low-carb Paleo diet. One part of stage I of catabolism is the breakdown of food molecules by hydrolysis reactions into the individual monomer unitsa€”which occurs in the mouth, stomach, and small intestinea€”and is referred to as digestionThe breakdown of food molecules by hydrolysis reactions into the individual monomer units in the mouth, stomach, and small intestine.. Disaccharides such as sucrose and lactose are not digested until they reach the small intestine, where they are acted on by sucrase and lactase, respectively.
The principal digestive component of gastric juice is pepsinogen, an inactive enzyme produced in cells located in the stomach wall. Since DHA is found in many tissues, the abnormalities in one tissue may share a similar biochemical cause as in other tissues. In animal studies it prevents skin cancer, kills ovarian cancer cells, and reduces diabetic complications such as cataracts. EPA levels were also elevated in the high-grade prostate cancers, but not by nearly as much as DHA levels. The trouble with this idea is that (a) this effect should have been strongest in the low-grade cancers, since diabetes reduced the incidence of low-grade cancers, but in the Brasky study DHA had no association with low-grade cancers, (b) fish oil lowers testosterone levels in rats, (c) in the Brasky study high-grade prostate cancers were strongly associated with obesity and the obese generally have low testosterone levels, and (d) surprisingly, high-grade prostate cancers are associated with low testosterone, not high. So cell membrane lipid measurements have the best chance to demonstrate a link to cancer risk. Angiogenesis does, in fact, drive the shift from low-grade to high-grade cancer, so a DHA-angiogenesis association would be consistent with this explanation. It could be the conscientious folks who followed bad diet advice from the hospital dietitian who got the high-grade cancers. It afflicts 35% of those over age 75, and is the leading cause of blindness in developed countries. Results from a recent clinical trial (5) also demonstrate that the progression of AMD can be slowed in some individuals by high daily doses of antioxidant vitamins and zinc. In this work we show that malignant melanoma cells are able to esterify all-trans retinol and subsequently isomerise all-trans retinyl esters into 11-cis retinol, whereas their benign counterparts – melanocytes are not able to catalyze these reactions. The major products of the complete hydrolysis of disaccharides and polysaccharides are three monosaccharide units: glucose, fructose, and galactose. When food enters the stomach after a period of fasting, pepsinogen is converted to its active forma€”pepsina€”in a series of steps initiated by the drop in pH. Chymotrypsin preferentially attacks peptide bonds involving the carboxyl groups of the aromatic amino acids (phenylalanine, tryptophan, and tyrosine). EPA and DHA appear together in fish and fish oil, so this suggests that fish consumption contributed to but was not the primary cause of the elevated tissue DHA. So one could argue that fish oil might promote high-grade prostate cancer by lowering testosterone! No effects were reported for cancers of the aerodigestive tract, bladder cancer, colorectal cancer, lymphoma, ovarian cancer, pancreatic cancer, or stomach cancer. Now, cancer is promoted by COX-2 pathway inflammation, which is why COX-2 inhibitors such as aspirin and ibuprofen are protective against cancer.
Direct evidence of oxidative damage in AMD donor eye tissues include elevated levels of CEP adducts uniquely derived from the oxidative fragmentation of DHA (6).
Unlike in wounds, where CEP is elevated for a few days, in cancers CEP elevation is chronic. Trypsin attacks peptide bonds involving the carboxyl groups of the basic amino acids (lysine and arginine). The drug finasteride greatly raised risk of high-grade prostate cancer, but the paper did not break down the DHA-cancer association between the finasteride and placebo arms.
In this largest study to date of vitamin A status and subsequent risk of prostate cancer, higher serum retinol was associated with elevated risk, with sustained high exposure conferring the greatest risk. CEP-driven angiogenesis may be an attractive therapeutic target, especially in cancers resistant to anti-VEGF therapy.
It has a fairly broad specificity but acts preferentially on linkages involving the aromatic amino acids tryptophan, tyrosine, and phenylalanine, as well as methionine and leucine. Pancreatic juice also contains procarboxypeptidase, which is cleaved by trypsin to carboxypeptidase. The most likely explanation, in my view, is that finasteride increases conversion of EPA to DHA and creates artificially high tissue DHA levels. Inflammation and oxidation-driven angiogenesis may occur in other pathologies, for example atherosclerosis, where arterial thickening can depend on its microvasculature. The latter is an enzyme that catalyzes the hydrolysis of peptide linkages at the free carboxyl end of the peptide chain, resulting in the stepwise liberation of free amino acids from the carboxyl end of the polypeptide.
The high DHA levels combined with oxidative stress drive cancer through the TLR-2 angiogenesis pathway.
This suggests that DHA has other effects, unrelated to its anti-inflammatory activity, that are cancer promoting.
In these settings, there is an extensive generation of oxidative products which might promote atherogenesis via TLR2. If DHA has pro-angiogenic effects that are independent of COX-2 mediated inflammation, then this could account for the observations. Thus, along with pathogen- and danger-associated molecular patterns, TLR2 recognizes an oxidation-associated molecular pattern. This new function of TLR2 as a sensor of oxidative stress reveals the shortcut link between innate immunity, oxidation and angiogenesis.




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