Immortalhair photos

Then I tried hardcore vegetable juicing which I think helped keep my hair but it was far too labor intensive and difficult with a busy work schedule.

mphatesmpb wrote:

Then I tried hardcore vegetable juicing which I think helped keep my hair but it was far too labor intensive and difficult with a busy work schedule.

CS,
Can you tell us more about your vegetable juicing regimen?

Gibson wrote:juicing is not the darker age IMO. it is a luxury if u can afford it. look at jack lalane, an advocate for juicing.

the only reason not t post pics on a hairloss forum is for obvious reasons of anonymity. on any other forum you will find plenty of pics because people are thriving and showing off--try raw food forums for pics.

It was the first thing I did in a mad obsession to control my hair loss. This was in the "darker age" of nutrition than I think we are in now. On the advice of juicing "guru," Jay Kordich, known as the Juiceman, I juiced the overwhelming majority of my juices as vegetable, consisting of three quarters carrot and one quarter green juices.

I focused on the most nutrient dense juices, such as Kale, Parsley and Cabbage, although I used a large variety of others such as Dandelion greens (quite bitter, but nutrient dense), Beets quite often (very robust and nutritious), and often used celery stalk in many. I believe these were the most important of the vegetables that I had used.

Vasorelaxing effects of flavonoids: investigation on the possible involvement of potassium channels.
Naunyn Schmiedebergs Arch Pharmacol. 2004.
A flavonoid-rich diet has been associated with a lower incidence of cardiovascular diseases, probably because of the antioxidant and vasoactive properties of flavonoids. Indeed, many flavonoids show vasorelaxing properties, due to different and often not yet completely clarified mechanisms of action. Among them, the activation of vascular potassium channels has been indicated as a possible pathway, accounting, at least in part, for the vasodilatory action of some flavonoid derivatives, such as apigenin and dioclein. Therefore, this work aims at evaluating, on in vitro isolated rat aortic rings, the endothelium-independent vasorelaxing effects of a number of flavonoid derivatives, to identify a possible activation of calcium-activated and/or ATP-sensitive potassium channels and to indicate some possible structure-activity relationships. Among the several flavonoids submitted to the pharmacological assay, only baicalein and quercetagetin were almost completely ineffective, while quercetin, hesperidin, quercitrin and rhoifolin exhibited only a partial vasorelaxing effect. On the contrary, acacetin, apigenin, chrysin, hesperetin, luteolin, pinocembrin, 4'-hydroxyflavanone, 5-hydroxyflavone, 5-methoxyflavone, 6-hydroxyflavanone and 7-hydroxyflavone, belonging to the chemical classes of flavones and flavanones, showed full vasorelaxing effects. The vasodilatory activity of hesperetin, luteolin, 5-hydroxyflavone and 7-hydroxyflavone were antagonised by tetraethylammonium chloride, indicating the possible involvement of calcium-activated potassium channels. Moreover, iberiotoxin clearly antagonised the effects of 5-hydroxyflavone, indicating the probable importance of a structural requirement (the hydroxy group in position 5) for a possible interaction with large-conductance, calcium-activated potassium channels. Finally, glibenclamide inhibited the vasorelaxing action of luteolin and 5-hydroxyflavone, suggesting that ATP-sensitive potassium channels may also be involved in their mechanism of action.

Influence of biotransformation of luteolin, luteolin 7-O-glucoside, 3',4'-dihydroxyflavone and apigenin by cultured rat hepatocytes on antioxidative capacity and inhibition of EGF receptor tyrosine kinase activity.
Schlupper D, Giesa S, Gebhardt R.
Source

Institute of Biochemistry, Medical Faculty, University of Leipzig, Leipzig, Germany.
Abstract

Flavonoids are known as biologically active compounds. Although this has been shown by several in vivo studies, it is still elusive whether their metabolites exert similar activities. Herein we investigated the biotransformation of four different flavonoids, 3',4'-dihydroxyflavone, apigenin, luteolin and luteolin 7-O-glucoside, by cultured rat hepatocytes using a combination of enzymatic deconjugation, HPLC separation and high-resolution mass spectrometry. These flavonoids were chosen because they are active components of many plants, e. g., artichokes. All flavonoids showed rather complex metabolite patterns dominated by phase II metabolites, mainly sulfates, methyl sulfates and methyl glucuronides, but also of combined glucuronide and sulfate conjugates. Phase I metabolism by hydroxylation was rendered likely only for apigenin to form luteolin. When culture media containing the flavonoids and their metabolites were assayed for antioxidative capacity by the DPPH assay, only compounds with hydroxy groups in position 3' and 4' of the B ring were active. Thus, during metabolism of (inactive) apigenin a strong increase in the antioxidative effect was observed while that of the other three flavonoids decreased with time. Determination of EGF receptor tyrosine kinase activity likewise revealed strong inhibition in the presence of a catechol group at ring B. However, in this case the situation was much more complex resulting in a significant increase of the inhibitory activity of 3',4'-dihydroxyflavone and apigenin, but not of luteolin and luteolin 7-O-glucoside during 22 h of incubation. These results show that the biotransformation of flavonoids is very complex and may result not only in a loss but also in a gain of biological activity depending on the individual structural features.

Designing a Cancer Fighting Diet
June 16, 2011 By alex

Over the last few years, cancer fighting diets have received a lot of attention due to the findings that certain plant phytochemicals (also known as: Nutraceuticals), can provide an additional means of regulating the genes and processes that drive the initiation and progression of cancer. In this article, we will show you how you can utilize combinations of nutraceuticals to greatly improve their performance.

Unfortunately, in order for nutraceuticals to inhibit cancer cells, they must be able to reach certain blood (plasma) concentrations, typically in the uM (micromolar) range. However, due to metabolic processes, the plasma concentration never naturally reaches higher than the nM (nanomolar) range. The amount and length of time a neutraceutical remains in the body is referred to as its bioavailability. The limited bioavailability of most nutraceuticals has been a significant roadblock to their clinical application.

However, there are approaches that can be used to increase the bioavailability of a nutraceutical and lower the plasma concentrations required for cancer fighting properties. In this article, we will show you how you can utilize combinations of nutraceuticals to greatly improve their performance. We will use the example of resveratrol, which is found in the skin of red grapes and other fruits, as it’s a commonly used nutraceutical that has been shown to have a proven role in inhibiting many cancers.

Although 70% of the resveratrol dose taken orally is absorbed by the body, the bioavailability of resveratrol is low because it is rapidly metabolized in the intestines and liver into conjugated forms (glucuronate and sulfonate). For example, with a 25 mg oral dose, only trace amounts (below 5 ng/mL) of free resveratrol can be detected in the blood. This is far below the amount required for its anti-cancer benefits to be realized. Furthermore, oral administration of doses higher than 3000 mg per kg of body weight can be dangerous.

Clearly, the low bioavailability of resveratrol limits its therapeutic use. However, it is possible to greatly improve resveratrol bioavailability by simultaneously incorporating other nutraceuticals that inhibit its metabolic break down.

There is a synergistic effect typically found when combining certain nutraceuticals that is most likely explained by an over-saturation of the metabolic enzymes and pathways that degrade these nutraceuticals individually. We can use this knowledge to improve the bioavailability of resveratrol in two ways:

* Through the use of combinations of nutraceuticals that specifically target the metabolic enzymes; and

* By over-saturating the metabolic enzymes, using phytochemicals that compete to bind to them.

The Metabolic Processes That Limit Resveratrol Bioavailability:

There are three processes that inhibit the bioavailability of most nutraceuticals and drugs. This occurs when they attempt to cross the barrier from the intestines into the blood vessels that go to the liver. Here they are removed by ABC transporters and phase 1/II enzymes, referred to as metabolic enzymes. If they do reach the liver, they are attacked by a higher concentration of these enzymes, in addition to monoamine oxidase enzymes (MAOs).

ABC Transporters:
These transporters pump nutraceuticals (and drugs) out of the barrier that exists between the intestines and the blood vessels (enterocytes), back into the intestines. Cancer cells increase the amount of ABC transporters such as breast cancer resistant protein (BCRP) and muti-drug resistance protein 2 (MDRP2).

Phase 1 Enzymes:
These enzymes target nutraceuticals and drugs with biochemical tags that allow them to be excreted. One phase 1 enzyme, CYP3A4, is responsible for metabolizing the majority of nutraceuticals and drugs.

Phase II Enzymes:
Phase II enzymes work by adding a sulfo-moiety (SULTs) or a B-glucuronide group (UGTs) to the target nutraceutical or drug. The tagged nutraceutical is then recognized by the ABC transporters and excreted back into the intestines.

MAO Enzymes:
These gut enzymes break down and inactivate nutraceuticals by removing functional components.

The following section outlines the metabolic processes involved in the breakdown of resveratrol and includes a selection of nutraceuticals that inhibit these processes. When the following nutraceuticals are combined in specific amounts, they greatly improve the bioavailability of resveratrol by inhibiting its breakdown and excretion.

ABC Transporters:
MRP2 – Inhibited by EGCG (green tea), Quercetin (Red onion), Apigenin (Parsley)

BCRP – Inhibited by Apigenin, Hesperetin (Peppermint), Naringenin (Rosemary)

Phase 1 Enzymes:
CYP3A4 – Inhibited by Naringenin, Kaempferol (Basil, Fennel), Grapefruit juice

Phase II Enzymes:
SULTs – Inhibited by Kaempferol, Apigenin, Genistein, Curcumin

UGTs – Inhibited by EGCG/Quercetin/BiochaninA, Curcumin (Tumeric), Piperine (Pepper)

MAO Enzymes:
MAOA – Inhibited by Quercetin, Harmine, Harmaline (grapes, avocados, blackcurrants)

Conclusion:

Including all types of nutraceuticals based on their characterized mechanism can maximize the synergistic effect and therefore lead to more of the cancer fighting properties of these substances getting through to your cells and therefore, directly influencing your cancer. Please contact us if you are interested in learning more about CTOAM’s personalized gene-targeted nutraceutical diets.

neurotrophils generate O2 and release lysozomal enzymes such as beta-glucuronidase [13]...We showed that luteolin monoglucuronide was hydrolyzed to free luteolin by beta-glucuronidase released from neurotrophils (Fig. 2). At inflammation site in vivo, pH is low. This pH is optimal for beta-glucuronidase...The concentration of this enzyme at inflammation site seems to be higher than that in whole blood. Therefore, released beta-glucuronidase might hydrolyze glucuronide conjugates of flavnoids to free aglycones in vivo.

Histology and cytochemistry of human skin. XI. The distribution of beta-glucuronidase.
MONTAGNA W.
Abstract
1. Various amounts of beta-glucuronidase activity may be found in all of the cutaneous appendages. 2. In the epidermis, the basal layer and the Malpighian layer contain a moderate amount of it, but a band of cells, including the stratum granulosum and the cells immediately above it, is rich in beta-glucuronidase. 3. The cells of the duct of eccrine sweat glands have moderately strong enzyme activity, but those in the secretory coil are strongly reactive; small and large reactive granules are crowded in the reactive cytoplasm. 4. The cells of the secretory coil of the apocrine glands contain more beta-glucuronidase than any other cutaneous appendage. 5. In the sebaceous glands, a very strong concentration of enzyme activity is found in the undifferentiated peripheral cells, a smaller amount of it is found in the differentiating cells. 6. In active hair follicles, the largest amount of beta-glucuronidase is found in the outer root sheath and in the bulb. In the outer sheath, the strongest concentration is found around the level of the keratogenous zone of the cortex. The dermal papilla is strongly reactive. In quiescent hair follicles, the outer root sheath has a moderate amount of enzyme concentration, but the dermal papilla is unreactive. 7. In the dermis, the fibroblasts in the papillary layer, the smooth muscle cells of the arrectores pilorum and the tunica media of arteries, and the fat cells all exhibit enzyme activity. Mast cells show a great concentration of beta-glucuronidase.