Lipodissolve Injections (Mesotherapy) are an injection of medication, homeopathic medicine, vitamins, plant extracts, or other substances directly into cells under the skin. Aesthetic Mesotherapy works by breaking up fat in cells that is then excreted through the body via the lymphatic system.
At Harbour Medispa Hamilton we inject exclusively Phosphatidylcholine (PC) and Sodium Deoxycholate (DC). PC is an emulsifier that makes up 40% of the human cell membrane. PC is a natural substance that is FDA + TGA approved for use in food and is also naturally found in egg yolks, as well as other foods. DC is a bile salt constituent that is made naturally in the human liver and used to break down the fats found in our food. When injected together, PC and DC work to break down the fat in our fat cells from a hard mass into a more liquid state that can then be passed through the body and eventually excreted.
Lipodissolve Injection is a minimally invasive procedure that is a great alternative to surgical liposuction. In fact, liposuction is proven to be ineffective at eliminating cellulite and it can often make cellulite more prominent. Liposuction works by removing fat cells, while Mesotherapy removes the fat from the fat cell; making it a very safe and effective alternative. Lipodissolve Injection patients experience no downtime, minimal bruising and pain, and are able to maintain their cellulite and fat loss with proper nutrition and exercise. Liposuction on the other hand is a surgical procedure, requiring two or more weeks of downtime, significant bruising and pain, weight gain in abnormal places post-procedure and many possible complications ranging from serious infection to possible death.
The results of Lipodissolve Injections are long-lasting. Follow-up procedures may be necessary for some patients. These follow-up procedures are done on an as-needed basis. To achieve maximum results, it is important for the patient to follow a healthy diet and exercise regimen. This is not a weight-loss strategy but rather a therapy to spot reduce fat.
Lipodissolve Injections can be used successfully on many trouble areas of the body including; love handles, stomach, saddlebags, bra bulge, inner thigh, inner and outer arms, buttocks, abdomen, double chin, face, neck, back, and waist. We understand that even with proper diet and exercise some areas of the body are just too stubborn. Whether you need to reduce cellulite for bikini season, tighten the abdomen post-baby, or just need a little chin reduction, Lipodissolve Injection is a safe, effective, and minimally invasive treatment for unwanted fat deposits. So there is no need to feel unhappy with these little trouble-spots or go under the knife to correct them.
Lipodissolve Injections Pre-Procedure Guidelines
Please read the instructions below carefully.
• Discontinue Anti-Inflammatory medication (eg Ibuprofen, Aspirin) at least 3-4 days before your procedure.
• Discontinue any blood thinners or any herbs, supplements, or vitamins 1-2 weeks before your procedure.
• Discontinue Systemic Steroids (Prednisone, Hydrocortisone, etc.) 1-2 weeks before your procedure. Steroid Injections (cortisone) should be discontinued at least 1 month before your procedure.
• Drink lots of water, especially on the day of your procedure.
If you have any questions, you are welcome to call the clinic mobile 0418 180 949 or send an SMS and we will reply to you
Lipodissolve Injections Post Procedure Guidelines
Please read the following steps carefully.
0-7 Days Post Lipodissolve Injection:
• It is recommended that the patient rest the day of the procedure. However, after the first 24 hours exercise is highly recommended to help achieve maximum results.
• A cool shower or compress will soothe any irritated areas.
• Drink at least 2L of water every day to help your body flush out fats that have been broken down. Water does not mean tea, coffee, sodas, or juice.
• Mild inflammation, bruising and tenderness may occur. Bruising may last from 3-7 days.
• It is normal for the localized fat in the treatment area to change consistency due to the bop layer of fat cells breaking down and leaving the cell walls.
• Do not consume alcoholic beverages for the first 7 days following your procedure.
• Avoid smoking. Smoking delays healing and can increase the risk of complications.
• DO NOT TAKE systemic steroids such as; Prednisone, Hydrocortisone, etc. for at least 2 weeks following your procedure.
• Do not take hot baths or go to saunas during the first few days following your procedure.
1-4 Weeks Post Lipodissolve Injection:
• Continue to increase your exercise, especially in the treated area of the body. Exercise will aid the body in fat burning after your procedure.
• Continue to drink 2L water every day to help your body flush out fats that have been broken down.
4 -6 Weeks Post Lipodissolve Injection:
• Your next Lipodissolve Injection session should be scheduled for 4-6 weeks after your procedure.
Anti Aging Foods | Promote Healthy Skin Aging From Inside
Discovering the link between nutrition and skin aging.
Skin has been reported to reflect the general inner-health status and aging. Nutrition and its reflection on skin has always been an interesting topic for scientists and physicians throughout the centuries worldwide. Vitamins, carotenoids, tocopherols, flavonoids and a variety of plant extracts have been reported to possess potent anti-oxidant properties and have been widely used in the skin care industry either as topically applied agents or oral supplements in an attempt to prolong youthful skin appearance. This review will provide an overview of the current literature “linking” nutrition with skin aging.
Beauty comes from the inside. The connection between nutrition and skin condition or rather the effect of nutrition on skin aging has been an interesting research field not only for scientists but also a common field of interest for humans throughout the years, from ancient times to nowadays. Skin aging consists of two didactically independent, clinically and biologically, distinct processes.1 The first is intrinsic skin aging, which represents chronological aging and affects skin in the same pattern it affects all internal organs.2 The second is extrinsic skin aging, which we view as aged skin and is the result of external factors and environmental influence, mainly chronic sun exposure and ultraviolet (UV) irradiation but also smoking, pollution, sleep deprivation and poor nutrition.
Prevention is the best and most effective way to work against extrinsic skin aging effects. The best prevention strategy against the harmful action of free radicals is a well regulated lifestyle (caloric restriction, body care and physical exercise for body), with low stress conditions and a balanced nutritional diet, including anti-oxidative rich food.
Frequently researched antioxidants such as carotenoids, tocophenols and flavonoids, as well as vitamins (A, C, D and E), essential omega-3-fatty acids, some proteins and lactobacilli have been referred as agents capable of promoting skin health and beauty.3,4 To find a proper balance, this review considers the beneficial “anti-aging” effects of increased reactive oxygen species (ROS) signaling recently.
The appropriate generation of ROS (for instance after physical exercise) has beneficial cell-protective and anti-aging effects. ROS activate via stimulation of STE-like 20 protein kinase 1 (MST1) and Jun N-terminus kinase (JNK) specific phosphorylations of forkhead box class O transcription factor (FoxO transcription factors), which thereafter translocate from the cytoplasm into the nucleus and thereby induce the expression of anti-oxidative enzymes like superoxide dismutase, catalase and others. The expression and upregulation of the cell’s own intrinsic antioxidative enzyme systems finally do the “job” and protect the cell against accumulating and harmful cellular levels of ROS.5 Remarkably, upregulation of nuclear FoxO levels suppresses cell proliferation and induces apoptosis.
The aim of this work is to review the existing literature and eventually to give an insight to the question whether diet actually influences the way our skin ages.
Vitamin C, also named L-ascorbic acid, is water soluble, photosensitive and is the most important antioxidant in the hydrophilic phase. Vitamin C is not naturally synthesized by the human body and therefore adequate dietary intake of vitamin C is required and essential for a healthy human diet.
The richest natural sources are fresh fruits and vegetables such as citrus fruits, blackcurrant, rose hip, guava, chili pepper or parsley. Stability of the vitamin C molecule depends on aggregate condition and formulation.
L-ascorbic acid can be used orally and topically for skin benefits. Vitamin C is a cofactor for lysyl and prolyl hydroxylase, which stabilize the triple helical structure of collagen.6 It also plays a role in cholesterol synthesis, iron absorption and increases the bioavailability of selenium. The most commonly described cutaneous manifestations accompanying vitamin C deficiency are attributed to the impaired collagen synthesis. Enlargement and keratosis of hair follicles mainly of the upper arms and curled hairs, the so-called ‘corkscrew hairs’, are usually described. The follicles become hemorrhagic with time and they sometimes mimic the palpable purpura of leucocytoclastic vasculitis.7
Additionally, vitamin C deficiency is known for causing scurvy, a disease with some manifestations such as fragility, skin lesions in form of petechiae, gum bleeding, ease of developing bruises or slow wound healing.8
Topically ascorbic acid is used in various cosmetic products, for example in lightening of skin dyspigmentation, anti-aging and sun protection formulations. The idea of sun protecting products is to have a combination product between a “passive” protection with a UV filter and an “active” protection with the antioxidant. UVB protection by vitamin C is frequently mentioned in the literature.6,9–11 However, the study by Wang et al. indicates that more work in formulation of cremes is needed, since there seem to be many products in which the desired effects are not measurable.12 The use of vitamin C in cosmetic products is difficult as its reducing capacity occurs very fast and its degradation may occur under the presence of oxygen even before the topical application to the skin.13
Nutricosmetic products with L-ascorbic acid work as free radical scavengers and repair the membrane bound oxidized vitamin E.14 A long-term study observed the effects of a combination of ascorbic acid and d-α-tocopherol (vitamin E) administered orally to human volunteers on UVB-induced epidermal damage. The treatment was well-tolerated and could be used prophylactically against the hazardous effects of solar UV irradiation and skin cancer, according to the authors.9 Another paper describes an 8-week study, which compared topical and systemic antioxidant treatment. Topical and systemic treatment both seemed to be good photoprotectants.15
There are many preparations of vitamin C- based products available on the market, but these are predominantly based on more stable esters and other derivatives of vitamin C which more readily penetrate the skin but are not necessarily converted to the only active vitamin C, L-ascorbic acid.16 These topical or oral products do not have the effects provided by L-ascorbic acid.
Tocopherols (vitamin E)
The vitamin E complex is a group of 8 compounds called tocopherols. Tocopherol is a fat-soluble membrane bound antioxidant and consequently a free-radical scavenger especially of highly reactive singlet oxygen. Tocopherol is like vitamin C a naturally occurring endogenous non-enzymatic antioxidant.
Vitamin C and vitamin E act synergistically. When UV-activated molecules oxidize cellular components, a chain reaction of lipid peroxidation in membranes rich in polyunsaturated fatty acids is induced. The antioxidant d-α-tocopherol is oxidized to the tocopheroxyl radical in this process and it is regenerated by ascorbic acid to d-α-tocopherol.17,18 Beside ascorbic acid, glutathione and coenzyme Q10 can also recycle tocopherol.
Higher amounts of tocopherol are available in vegetables, vegetable oils like wheat germ oil, sunflower oil, safflower oil and seeds, corn, soy and some sorts of meat. The intake of natural vitamin E products helps against collagen cross linking and lipid peroxidation, which are both linked to aging of the skin.
With the process described above, D-α-tocopherol is involved in stabilizing the cell membrane by inhibiting oxidation of polyunsaturated fatty acids, such as arachidonic acid of membrane phospholipids. Topical applied vitamin E is described to reduce erythema, sunburned cells, chronic UVB-induced skin damage and photocarcinogenesis in the majority of the published studies.13,19 Vitamin E deficiency has been associated with a syndrome of edema with papular erythema or seborrhoiec changes, dryness and depigmentation in premature infants.20
There are many clinical studies, which have tested the effects of tocopherol. The data seem to be controversial, but high doses of oral vitamin E may affect the response to UVB in humans.21 Data of Ekanayake-Mudiyanselage and Thiele suggest that vitamin E levels are dependent on the density of sebaceous glands in the skin. In a 3-week study with daily oral supplementation of moderate doses of α-tocopherol significantly increased vitamin E levels measured in skin sites rich in sebaceous glands, such as the face. This should be considered when designing clinical vitamin E studies.22
Oral combination treatments of vitamins C and E, partly with other photoprotective compounds, did increase the photoprotective effects dramatically compared with monotherapies. Experts recommend that this synergetic interplay of several antioxidants should be taken into consideration in future research on cutaneous photoprotection.23
Carotenoids (vitamin A, β-carotene, astaxanthin, retinol)
Carotenoids are vitamin A derivates like β-carotene, astaxanthin, lycopene and retinol, which are all highly effective antioxidants and have been documented to possess photoprotective properties. Findings of Scarmo et al. suggest that human skin, is relatively enriched in lycopene and β-carotene, compared with lutein and zeaxanthin, possibly reflecting a specific function of hydrocarbon carotenoids in human skin photoprotection.24
β-carotene is the most prominent member of the group of carotenoids, natural colorants that can be found in the human diet.25 Compared with other carotenoids, the primary role of β-carotene is its provitamin-A activity. β-carotene can be cleaved by BCMO1 enzyme into 2 molecules of all-trans-retinal. There is no difference between naturally occurring and chemically synthesized β-carotene. Furthermore, β-carotene can also act as a lipid radical scavenger and as a singlet oxygen quencher, as demonstrated in vitro.26 Based on the distribution of BCMO1 in human tissues it seems that β-carotene metabolism takes place in a wide variety of organs, including the skin.27
Carrots, pumpkin, sweet potatoes, mangos and papaya are some examples of β-carotene containing fruits and vegetables.
Upon dietary supplementation, β-carotene can be further enriched in skin, in which it is already a major carotenoid.28 β-carotene is an endogenous photoprotector, and its efficacy to prevent UV-induced erythema formation has been demonstrated in various studies.29,30 In healthy volunteers, a 12-week oral administration of β-carotene may result in a reduction of UV-induced erythema.31 Similar effects have been described in volunteers receiving a lycopene-rich diet.32
The systemic photoprotecting effect of β-carotene depends both on dose and duration of treatment. In studies documenting protection against UV-induced erythema, supplementation with carotenoids lasted for at least 7 weeks, with doses > 12 mg/d of carotenoids.31,33–35 With treatment periods of only 3–4 weeks, studies reported no protective effects.36 Furthermore, β-carotene supplementation can significantly reduce the rate of mitochondrial mutation in human dermal fibroblasts after UV irradiation.37
Astaxanthin is found in microalgae, yeast, salmon, trout, krill, shrimp, crayfish and crustacea. Astaxanthin is biosynthesized by microalgae or phytoplankton, which are consumed by zooplankton or crustacea. They accumulate astaxanthin and, in turn are ingested by fish which then accrue astaxanthin in the food chain.38 Therefore, astaxanthin has considerable potential and promising applications in human health and nutrition39 and has been attributed an extraordinary potential for protecting the organism against a wide range of diseases (reviewed in refs. 40 and 41).
The UV protective effects of algal extract containing 14% of astaxanthin compaired to synthetic astaxanthin have also been tested. The authors of this study reported that preincubation with synthetic astaxanthin or an algal extract could prevent UVA-induced alterations in cellular superoxide dismutase activity and decrease in cellular glutathione content.42
In a study of Camera et al. the modulation of UVA-related injury by astaxanthin, canthaxanthin, and β-carotene for systemic photoprotection in human dermal fibroblasts has been compared.43 Astaxanthin showed a significant photoprotective effect and counteracted UVA-induced alterations to a great extent. The uptake of astaxanthin by fibroblasts was higher than that of canthaxanthin and β-carotene, which lead to the assumption that the effect of astaxanthin toward photooxidative changes was stronger than that of the other substances. A recent study of Suganuma et al. showed that astaxanthin could interfere with UVA-induced matrix-metalloproteinase-1 and skin fibroblast elastase/neutral endopeptidase expression.44 Both studies suggest that effects of UVA radiation, such as skin sagging or wrinkling can be prevented or at least minimized by topical or oral administration of astaxanthin.36,42,44
Lycopene is a bright red carotene and carotenoid pigment and phytochemical found in tomatoes and other red fruits and vegetables, such as red carrots, watermelons and papayas (but not strawberries or cherries). Although lycopene is chemically a carotene, it has no vitamin A activity.
β-carotene and lycopene are usually the dominating carotenoids in human blood and tissues and are known to modulate skin properties when ingested as supplements or as dietary products. While they cannot be compared with sunscreen, there is evidence that they protect the skin against sunburn (solar erythema) by increasing the basal defense against UV light-mediated damage.45
A study confirmed that the amounts of lycopene in plasma and skin are comparable to or even greater than those of β-carotene. When skin is exposed to UV light stress, more skin lycopene is destroyed compared with β-carotene, suggesting a role of lycopene in mitigating oxidative damage in tissues.46 Lycopene and tomato products are also mentioned for preventing cancer.47,48
Retinol is important for the human body; however the body itself cannot synthesize it. Retinol, a fat-soluble unsaturated isoprenoid like its two important metabolites retinaldehyde and retinoic acid, is essential for growth, differentiation and maintenance of epithelial tissues and influences reproduction. In human skin two retinoid receptors are expressed, which can be activated by retinol and its metabolites.49
Retinaldehyde, additionally being important for vision, is created by in vivo oxidation of retinol in a reversible process. The normal plasma concentration of vitamin A in humans is 0.35–0.75 μg/ml.50,51
Retinol must derive from diet. Natural retinol and retinol ester are contained in liver, milk, egg yolk, cheese and fatty fish etc. Naturally occurring and synthetic vitamin A (retinol) show similar biological activities. Different retinol products, both for cosmetic (topical) and pharmaceutical (topical, systemic) use can be found on the market.
In a review of topical methods to counteract skin wrinkling and irregular pigmentation of aging skin, Bayerl evaluates the effects of vitamin A acid derivatives, chemical peeling and bleaching agents. Also, the effects of UV protection by using sunscreens and topical antioxidants are reviewed.52 The topical retinoid treatments inhibit the UV-induced, MMP-mediated breakdown of collagen and protect against UV-induced decreases in procollagen expression.53–55
Endogenous retinoids cannot be linked to the pathogenesis of common skin diseases like acne and psoriasis. Oral treatment with retinol or retinal derivatives has not been proposed as a possible anti-aging treatment. Humans require 0.8‒1 mg or 2400‒3000 IU vitamin A per day (1 IU = 0.3 µg).51
Unfortunately the large CARET trial mentioned lung cancer-promoting effects of 25,000 IU retinyl palmitate combined with 30 mg β-carotene intake in smokers.56 Thus, the belief that chemical quenching of free radicals by natural compounds like retinyl palmitate and β-carotene exerts always beneficial effects has been challenged. Omenns data showed that an artificial systemic increase of antioxidants by dietary supplementation intended to modify UV erythema thresholds may have severe internal adverse effects which even may not only increase risk of cell aging but of tumor promotion. However experts still recommend dietary intake of fruits and vegetable.
In humans vitamin D serves two functions, it acts as a prohormone and the human body can synthesize it itself through sun exposure. Skin is the major site for UV-B mediated vitamin D3, and 1,25-dihydroxy vitamin D3 synthesis. Smaller amounts of vitamin D2 and D3 come from the dietary intake of animal-based foods such as fatty fish or egg yolk. Some products like milk, cereals and margarine can be enriched with vitamin D.
Excess of vitamin D is stored in fat of the body and can result in toxic effects. This toxicity presents with nausea, vomiting, poor appetite, weakness, weight loss and constipation. Food-intake of vitamin D high enough to cause toxicity is very unlikely.
The skin is one of the key tissues of the human body vitamin D endocrine system. It is important for a broad variety of independent physiological functions, which are reviewed in Reichrath et al.51 Besides its role in calcium homeostasis and bone integrity 1,25-dihydroxy vitamin D3 [1,25(OH)2D3] is also essential for numerous physiologic functions including immune response, release of inflammatory cytokines and regulation of growth and differentiation in normal and malignant tissues such as breast, lung and colon.51 1,25(OH)2D3 protects human skin cells from UV-induced cell death and apoptosis,57 inhibits the activation of stress-activated protein kinases,58 such as the c-Jun NH2-terminal kinase and p38, and suppresses IL-6 production. Several in vitro and in vivo studies have documented the protective effect of 1,25(OH)2D3 against UVB-induced skin damage and carcinogenesis.58,59 Furthermore, 1,25(OH)2D3 induces the expression of antimicrobial peptide genes in human skin60 and plays a significant role in preventing opportunistic infections. With increasing age the capacity of the skin to produce vitamin D3 declines and consequently the protective effects of the vitamin. There are several factors contributing to this deficiency state among them behavioral factors, for example limited sun exposure or malnutrition, which can be partially altered by behavior modification and various intrinsic factors like reduced synthetic capacity. In skin, the concentration of 7-dehydrocholesterol—a vitamin D3 precursor—showed an approximately 50% decline from age 20 y to age 80 y61 and the total amount of pre-vitamin D3 in the skin of young subjects was at least two times greater than when compared with that of the elderly subjects. Vitamin D and calcium supplementation is therefore of great importance in the elderly population.13
Chang et al. also suggest an association between skin aging and levels of 25(OH)D3, another precursor of vitamin D. It may be possible that low 25(OH)D3 levels in women, who show less skin aging may reflect underlying genetic differences in vitamin D synthesis.62
Many other studies that tested oral vitamin D treatment showed skin cancer prevention, which is linked to anti-aging effects.63,64
In 2009, the American Academy of Dermatology and the Canadian Cancer Society recommended a 200 IU/day dosis for children (0–14 y), 200 IU for the age population between 14–50 y, 400 IU for the 50–70 y and 600 IU for people over their 71st year of age.65
A higher dose of vitamin D 1000 IU/day (adults) and 400 IU/day (children 0–14 y) intake has been recommended for individuals with known risk factors for vitamin D insufficiency like dark skin individuals, elderly persons, photosensitive individuals, people with limited sun exposure, obese individuals or those with fat malabsorption.65
The Food and Nutrition Board published a new recommendation for dietary allowance levels and tolerable upper intake levels (ULs) for vitamin D intake in 2010. The recommended dietary allowance (Table 1) represents a daily intake that is sufficient to maintain bone health and normal calcium metabolism in healthy people.66
Recommended dietary allowances for vitamin D
400 IU (10 mcg)
400 IU (10 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
600 IU (15 mcg)
800 IU (20 mcg)
800 IU (20 mcg)
*AI, Adequate Intake; IU, international unit; mcg, microgram, 40 IU = 1 mcg.
Long-term intakes of vitamin D above the upper intake levels increase the risk of adverse health effects. Most reports suggest a toxicity threshold for vitamin D of 10,000 to 40,000 IU/day and serum 25(OH)D levels of 500–600 nmol/L (200–240 ng/mL).
With daily intakes below 10,000 IU/day, toxicity symptoms are very unlikely. However, recent results from observational studies, national survey data and clinical trials have shown adverse health effects over time at much lower levels of vitamin D intakes and serum 25(OH)D. Since serum levels of approximately 75–120 nmol/L or 30–48 ng/mL have been associated with increased all-cause mortality, greater risk of cancer at some sites like the pancreas, greater risk of cardiovascular events as well as more falls and fractures with elderly subjects, the Food and Nutrition Board advises that serum 25(OH)D levels above 125–150 nmol/L (50–60 ng/mL) should be avoided and cites research results that link vitamin D intakes of 5,000 IU/day with a serum concentration at a maximum of 100–150 nmol/L (40–60 ng/mL).66
Polyphenols have drawn the attention of the anti-aging research community over the last decade, mainly because of their antioxidant properties, their great intake amount in our diet and the increasing studies showing their probable role in the prevention of various diseases associated with oxidative stress, such as cancer and cardiovascular and neurodegenerative diseases.67 Their total dietary intake could be as high as 1 g/d, which is much higher than that of all other classes of phytochemicals and known dietary antioxidants.68,69 They are mostly found in fruits and plant-derived beverages such as fruit juices, tea, coffee, and red wine. Vegetables, cereals, chocolate and dry legumes are also sources for the total polyphenol intake.69 Several thousand molecules having a polyphenol structure have been identified in plants being generally involved in defense against UV radiation or aggression by pathogens. Depending on the number of phenol rings and the way that these rings bind to one another, polyphenols can be divided into many different functional groups such as the phenolic acids, flavonoids, stilbenes, and lignans.67 Flavonoids are also further divided into flavones, flavonols, isoflavones, and flavanones, each with a slightly different chemical structure.6
It has been reported that the polyphenolic content of foods can be easily affected or seriously reduced by methods of meal preparation and culinary traditions. For example, onions, which are a major source of phenolic acids and flavonoids, and tomatoes lose between 75% and 80% of their initial content when boiled over 15 min, 65% when cooked in a microwave oven and 30% when fried.70 In French fries or freeze-dried mashed potatoes no remaining phenolic acids were to be found.71
Laboratory studies of different polyphenols such as, green tea polyphenols, grape seed proanthocyanidins, resveratrol, silymarin and genistein, conducted in animal models on UV-induced skin inflammation, oxidative stress and DNA damage, suggested that these polyphenols, combined with sunscreen protection, have the ability to protect the skin from the adverse effects of UV radiation, including the risk of skin cancers.72 The underlying mechanism of polyphenols actions has been a major discussion over the last decades. One of the most abundant theories is that the cells respond to polyphenols mainly through direct interactions with receptors or enzymes involved in signal transduction, which may result in modification of the redox status of the cell and may trigger a series of redox-dependent reactions.73,74 As antioxidants, polyphenols may improve cell survival; as prooxidants, they may induce apoptosis and prevent tumor growth.69,75 However, the biological effects of polyphenols may extend well beyond the modulation of oxidative stress.69
Some interesting polyphenols, flavonoids and botanical anti-oxidants and their properties, which have drawn attention for their unique anti-aging effects are discussed next.
Phlorizin belongs to the group of dihydrochalcones, a type of flavonoids and it is naturally occurring in some plants. It could be found in the bark of pear (Pyrus communis), apple, cherry and other fruit trees. It has been used as a pharmaceutical and tool for physiology research for over 150 y. However, its anti-aging effects have only been reported in the last years. Investigations of the effects of phlorizin on lifespan of the yeast Saccharomyces cerevisiae showed an improvement of the viability of the yeast, which was dose-dependent under oxidative stress.76 Further investigations on humans are needed.
Many other botanical extracts, which are not discussed in this review, have been described to have potent anti-oxidant properties. Among them silymarin,77 apigenin78 and genistein79 have been demonstrated to have beneficial effects on skin aging parameters.
The nutrient-sensitive kinase mammalian target of rapamycin complex 1 (mTORC1) integrates nutrient signaling. This mTORC1 is the central hub regulating protein and lipid synthesis, cell growth and cell proliferation and the process of autophagy and is thus intimately involved in central regulatory events associated with cell survival and cell aging. Intriguingly, all natural plant-derived polyphenols like EGCG, resveratrol, curcumin, genestin and others are natural inhibitors of mTORC1, recently described in this journal.80 Natural polyphenols exert their major metabolic activity as mTORC1 inhibitors, a fundament aspect relating calorie restriction and/or nutrient-derived mTORC1 attenuation to deceleration of aging. In fact, it has recently been demonstrated that mTORC1 inhibition by rapamycin extended life span in mice.81 This antioxidants from naturals souce exhibit more crucial functions as “Botanical mTORC1 inhibitors” and attenuate mTORC1 signaling, a beneficial property which decelerates cell metabolism, energy expenditure, mitochondrial activity and thus total ROS generation and oxidative stress load of the cells.
Resveratrol is an antioxidant, natural polyphenol, abundant in the skin of grapes (but not in the flesh). It has been the subject of intense interest in recent years due to a range of unique anti-aging properties. High concentrations of natural resveratrol and resveratrol oligomeres are found in grape shoots from Vitis Vinifera. Resveratrol and its oligomeres, trans-piceatannol, the dimers epsilon-viniferin, ampelopsin, iso-epsilon-viniferin, the trimers miyabenol C and the tetramers hopeaphenol, R-viniferin and R2-viniferin belong to the sub-group of stilbenes. Resveratrol works both as a chelating agent and as a radical scavenger and in addition it takes part in inflammation by inhibiting the production of IL-8 by LPS-induced MAPK phosphorylation and a block of NFΚB activation.82 In 2002 Bhat et al. reported that resveratrol possesses cancer chemopreventive activities.83 Cardiovascular benefits via increased nitric oxide production, downregulation of vasoactive peptides, lowered levels of oxidized low-density lipoprotein, and cyclooxygenase inhibition; possible benefits on Alzheimer disease by breakdown of β-amyloid and direct effects on neural tissues; phytohormonal actions; antimicrobial effects; and sirtuin activation, which is believed to be involved in the caloric restriction-longevity effect have also been reported.84 As far as skin is concerned, resveratrol has been recently shown to possess a protective action in vitro against cell death after exposure of HaCaT cells to the nitric oxide free radical donor sodium nitroprusside.85 Furthermore, Giardina et al. reported in 2010 that in experiments in vitro with skin fibroblasts treated with resveratrol there was a dose-related increase in the rate of cell proliferation and in inhibition of collagenase activity.86 Steinberg showed that resveratrol oligomers hopeaphenol, epsilon-viniferin, R2-viniferin, ampelopsin inhibit the growth number of human tumor cell lines significantly stronger than resveratrol itself.87,88
Curcumin is the principal curcuminoid of the popular Indian spice turmeric, which is a member of the ginger family (Zingiberaceae) and is frequently found in rice dishes to add yellow color to the otherwise white rice. Curcumin has been shown to protect against the deleterious effects of injury by attenuating oxidative stress and suppressing inflammation (reviewed in ref. 89). In human fibroblasts curcumin induced cellular stress responses through phosphatidylinositol 3-kinase/Akt pathway and redox signaling, thus providing evidence that curcumin-induced hormetic stimulation of cellular antioxidant defenses can be a useful approach toward anti-aging intervention.90 Oral ingestion in rodents has produced correction of cystic fibrosis defects and inhibition of tumor proliferation, but human trials are lacking.6,91,92
Green tea polyphenols
Green tea polyphenols (GTPs) derivating from the leaves of the Camellia sinensis have been postulated to protect human skin from the cutaneous signs of photoageing. In animal models, UV-induced cutaneous edema and cyclooxygenase activity could be significantly inhibited by feeding the animals with GTPs.93 However, in a study in 2005, although participants treated with a combination regimen of topical and oral green tea showed histologic improvement in elastic tissue content, clinically significant changes could not be detected.94 Many laboratories have reported that topical treatment or oral consumption of green tea polyphenols inhibits chemical carcinogen- or UV radiation-induced skin tumorigenesis in different animal models. Studies have shown that green tea extract also possesses anti-inflammatory activity. These anti-inflammatory and anti-carcinogenic properties of green tea are due to their polyphenolic constituents present therein. The major and most chemopreventive constituent in green tea responsible for these biochemical or pharmacological effects is (-)-epigallocatechin-3-gallate (EGCG).95 EGCG can directly inhibit the expression of metalloproteinases such as MMP-2, MMP-9 and MMP-12,96 and is a potent inhibitor of leucocyte elastase,97 which is instrumental in tumor invasion and metastasis.
Topical application of green tea extract containing GTPs on C3H mice reduced UVB- induced inflammation.98 The researchers also found protection against UV-induced edema, erythema, and antioxidant depletion in the epidermis. This work further investigated the effects of GTPs after application to the back of humans 30 min before UV irradiation. A decrease of myeloperoxidase activity and infiltration of leukocytes compared with the untreated skin was documented.99
Coenzyme Q10 (CoQ10) is a fat-soluble, endogenous (synthesized by the body), vitamin-like substance that is mainly stored in the fat tissues of our body. It is present in most eukaryotic cells, primarily in the mitochondria and plays an important role as a component of the electron transport chain in the aerobic cellular respiration, generating energy. Ubiquinol is also a well-known powerful antioxidant compound. In the skin, CoQ10 is mainly to be found in the epidermis where it acts in combination with other enzymic and non-enzymic substances as the initial barrier to oxidant assault.100 Primary dietary sources of CoQ10 include oily fish (such as salmon and tuna), organ meats (such as liver), and whole grains. The amount of CoQ10 needed in human organism can be gained through a balanced diet, however in the market CoQ10 is available in several forms as a supplement, including soft gel capsules, oral spray, hard shell capsules, and tablets. As a fat-soluble substance it is better absorbed when taken with fat rich meals. CoQ10 is also added to various cosmetics. It has been shown on rats that a CoQ supplementation elevates CoQ homologs in tissues and their mitochondria, thus causing a selective decrease in protein oxidative damage, and an increase in antioxidative potential.101 Furthermore, in a human study where 50 mg each of vitamin E, coenzyme Q10, and selenium were administered combined with the use of topical bio-cosmetics, an increase in stratum corneum CoQ10 was noted after 15 and 30 d of ingestion.102 In cases of primary CoQ10 deficiency in vitro experiments have shown that they should be treated with CoQ10 supplementation and that complementary administration of antioxidants with high bioavailability should be considered if oxidative stress is present.103 On the other hand, in experiments contacted on mice the supplemental intake of CoQ10 had no effect on the main antioxidant defense or pro-oxidant generation in most tissues, and had no impact on the life span of mice.104
The term probiotic is defined as “living microorganisms, which, when consumed in adequate amounts, confer a health effect on the host.”105,106
The most commonly used probiotics in humans and animals are enterococci, lactobacilli and bifidobacteria, which are natural residents of the intestinal tract.
A prebiotic is a non-viable food component that confers a health benefit on the host associated with modulation of the microbiota.107 Oligofructose and other oligosaccharides are prebiotic which have a significant effect on the population of luminal flora, in particular, stimulating bifidobacterial populations.
Currently, finding alternatives to antibiotics for skin treatment is receiving a lot of interest in research. It has been found that, similarly to the gut microflora, the skin’s microbiota plays a beneficial role. Thus, the possibility to modulate the microbiota more selectively is highly interesting.
UV exposure is known to negatively affect immune system functions.108 Clinical studies that used probiotic bacteria (Lactobacillus johnsonii NCC 533) to modulate the cutaneous immune homeostasis altered by solar-simulated UV exposure in humans suggest that certain probiotics can help preserve the skin homeostasis by modulating the skin immune system.109,110
According to Schouten et al., a prebiotic diet caused reduced acute allergic skin response in recipient mice.111
Essential fatty acids (EFAs) are long-chain polyunsaturated fatty acids derived from linolenic, linoleic and oleic acids. They cannot be produced in the human body and they have to be consumed through our daily dietary intake. EFAs have also been known as vitamin F. Arachidonic acid is a semi-EFA, as it can be synthesized in the body from linoleic acid. The two families of EFAs are ω-3, derived from linolenic acid, and ω-6, derived from linoleic acid, with the number indicating the position of the first double bond continuing from the terminal methyl group on the molecule.6,112 They are present in multiple food sources such as fish and shellfish, flaxseed, hemp oil, soya oil, canola oil, chia seeds, pumpkin seeds, sunflower seeds, leafy vegetables, walnuts, sesame seeds, avocados, salmon and albacore tuna. EFAs are essential for the synthesis of tissue lipids, play an important role in the regulation of cholesterol levels and are precursors of prostaglandins.113
The association between nutrient intakes and skin aging has been examined in 2008 in 4025 women (40–74 y), using data from the first National Health and Nutrition Examination Survey. Skin-aging appearance was defined as having a wrinkled appearance, senile dryness, and skin atrophy. Higher linoleic acid intakes were associated with a lower likelihood of senile dryness and skin atrophy.114 In a study where the effect of fish oil on UV (UV) B-induced prostaglandin metabolism was examined, 13 patients with polymorphic light eruption received dietary supplements of fish oil rich in omega-3 polyunsaturated fatty acids for 3 mo. The authors managed to show a reduction in UV-induced inflammation, possibly due to lowered prostaglandin-E2 levels.115 Furthermore, oral administration of an antioxidant mixture containing vitamin C, vitamin E, pycnogenol and evening primrose oil significantly inhibited wrinkle formation caused by chronic UVB irradiation through significant inhibition of UVB-induced matrix metalloproteinase (MMP) activity accompanied by enhancement of collagen synthesis on hairless mouse skin.116
EFAs can also be found as artificial supplements in the market. Fish oil supplements are usually made from mackerel, herring, tuna, halibut, salmon, cod liver, whale blubber, or seal blubber, are rich in omega-3 fatty acids and often contain small amounts of vitamin E. They might be also combined with calcium, iron, or vitamins A, B1, B2, B3, C or D.
It is widely accepted that caloric restriction (CR), without malnutrition, delays the onset of aging and extends lifespan in diverse animal models including yeast, worms, flies, and laboratory rodents.117 Although the underlying mechanisms remain still unknown, some explanations such as alterations of hormone metabolism, hormone-related cellular signaling, oxidation status, DNA repair, apoptosis, and oncogene expression, have been postulated.118,119 In a histological study on Fischer 344 rats undergoing dietary CR, the histomorphological changes resulting from intrinsic aging were delayed or prevented by CR. Namely, a trend toward increased values for collagen and elastic fibers, fibroblasts, and capillaries and a prevention of age-related increase in the depth of the epidermis, dermis, and fat layer was observed in skin samples from CR rats.120 Furthermore, in skin tissues of mice with CR weight control a palette of genes showed a differential expression when compared with mice receiving normal diet. The authors concluded that dietary CR showed profound inhibitory impact on the expression of genes relevant to cancer risks.121 Studies evaluating CR in nonhuman primates and its effects on human health, and on the metabolic parameters are ongoing.
To conclude, nutrition and skin aging still remains a controversial and conflicting subject. A promising strategy for enhancing skin protection from oxidative stress is to support the endogenous antioxidant system, with antioxidants containing products that are normally present in the skin.11 However, this should be not confused with a permanent intake of non-physiological high dosages of isolated antioxidants. Fruit and vegetables consumption may represent the most healthy and safe method in order to maintain a balanced diet and youthful appearing skin.
When metabolized, alcohol produces free radicals, which are chemicals in the skin that injure our precious collagen. These collagen fibers keep our skin firm and structured. Think of alcohol’s free radicals ingest collagen, poking little holes in those fibers. And when you lose collagen the consequences are fine lines, wrinkles and laxity. In fact, like sun exposure, alcohol breaks down collagen.
The Fix: Antioxidant creams and serums applied to the skin. Use them daily for best results, but definitely at bedtime if you drank alcohol. Antioxidants are the cure to free radicals. They effectively cut those damaging results produced by alcohol to save collagen and prevent wrinkles, fine lines and laxity. Vitamin C serum is a source of very powerful antioxidant you should incorporate into your skin routine. Ounce for ounce it’s simply the nuke of antioxidants. If you’re planning to drink, apply it in the morning to protect and at night to treat.
And it’s a good idea to also take supplements like omega–fatty–acids (fish oils) as well as lycopene and glutathione. At dinner, with your drink, order green vegetables or berries for dessert, as they are loaded with antioxidants. And instead of that venti iced coffee order a green tea!
Vitamin C Serum
Vitamin C Active serum is available in clinic at Harbour Medispa, Hamilton
Live Now is an active skincare range designed for busy modern women which will help reduce the build-up of excess oil and dead skin cells, normalize the function of cell renewal, reduce inflammation, and prevent bacteria formation deep within the hair follicle and pores.
Constantly I am asked in Wilston cosmetic clinic about Retin A and Retinol for acne and antiageing. I will often explain what the differences are between the two products. There are a number of posts I have supplied on my blog explaining about Retin-A and Retinol, today, I am exploring Tretinoin which is a form of Retin A.
Topical tretinoin is a generic form of acne medication Retin-A. Tretinoin can be purchased with a prescription from a Doctor or at a medical cosmetic clinic.
Typically, topical tretinoin is both a short-term solution and long-term treatment option for clearing up active breakouts. It’s used for hard-to-clear acne blemishes on your skin.
Tretinoin is effective for many people, but it’s not for everyone. Keep reading to find out what you should know before trying tretinoin for your acne.
Tretinoin is a retinoid, meaning it’s a form of vitamin A. Retinoids stimulate cell turnover on your skin. Dead skin cells are cleared off your skin more quickly as new skin cells rise to the surface. Quicker cell turnover opens your pores, releasing trapped bacteria or irritants that are causing your acne.
Retinoids like tretinoin also help your skin to regulate its natural oil (sebum) production, which can prevent future breakouts. They also have anti-inflammatory properties that clear up active acne pustules.
Tretinoin for wrinkles
Tretinoin has been studied extensively for its impact on the visible signs of aging. Tretinoin cream has demonstrated both short-term and long-term effects on the appearances of wrinkles, that’s why tretinoin is a popular ingredient in many over-the-counter face and eye creams albeit in much lower doses.
Tretinoin for acne scars
Tretinoin can also be used to decrease the appearance of acne scarring. Since tretinoin speeds up cell turnover on your skin, it can encourage new cell growth at the site of scarring.
Tretinoin in several forms has been tested successfully as an effective way to treat acne scars. Tretinoin is also sometimes used to prep skin for chemical peel treatments that target scarring.
Using tretinoin for acne can cause side effects. Not everyone will experience all of the side effects, and some may be more severe than others. Possible side effects include:
burning or itching skin
peeling or redness on your skin
unusual dryness of your skin
skin that feels warm to the touch
skin that turns a lighter color at the site of application
It can take up to 12 weeks to see results from using tretinoin. If your skin seems irritated by using it, check with a medical professional to see if symptoms are within the range of what’s normal for tretinoin.
If, after 8 to 12 weeks, you don’t see any improvement in your skin, speak with a medical professional. Tretinoin is not recommended for people who are pregnant or breastfeeding.
When you’re using tretinoin, be extra careful about your exposure to the sun and ensure you wear sunscreen whenever you’re going outside. Also additional preventative measures like wearing a hat with a broad brim.
It’s extremely rare but possible to overdose on tretinoin. Overdoses are more likely to occur in prescription-strength forms of this medication (such as Retin-A). Signs of an overdose include having trouble breathing or losing consciousness.
If you feel like you’re having an allergic reaction or experiencing serious side effects from tretinoin, discontinue use and seek medical attention immediately.
Other topical acne medications can interact with tretinoin and irritate your skin or aggravate side effects like burning on your skin. Unless they’re part of a plan you’ve discussed with your medical professional, avoid using other topical skin treatments (such as benzoyl peroxide, salicylic acid, and products containing sulfur) while using tretinoin. Also, avoid products that dry your skin, such as astringents and cleansers that contain alcohol.
Notably, tretinoin concentrations less than 0.01% are largely ineffective in the treatment of photodamaged skin (16-18). Topical application of other retinoids, such as isotretinoin and retinol also lead to clinical improvements, again with less skin irritation and after a much longer exposure time than tretinoin (19).
If you want to use tretinoin to treat acne, start by choosing a cream or gel that has a low amount (0.1 percent) of the active ingredient tretinoin. If needed, you can work up to higher amounts as your skin becomes accustomed to the treatment.
To apply tretinoin safely and effectively:
Clean your skin with warm water and pat dry before using any topical acne medication. Wash your hands before applying any cream or lotion to your face. Wait a few minutes to make sure your skin is completely dry before you use the medication.
Apply just enough of the medication to lightly cover the affected area. You don’t need to build a thick layer of the medication on your face. A dime-size amount of the medication should be enough to spread across your whole face.
Using the tips of your fingers, spread the medication away from sensitive areas such as your eyes, your nostrils, and your lips. Rub the cream or gel in to your face lightly and let it absorb completely.
For best results, apply tretinoin once at bedtime so that it can absorb completely into your skin while you sleep. It’s best not to apply makeup in the hours immediately following this treatment.
The No-BS Guide to Getting Natural-Looking Cosmetic Injectables
Everything you need to know about how a clinic will fix your wrinkles and give you back your youth
Inevitably, everyone will have a moment like this: You’re working on a new eyeliner trick or you catch a glimpse of yourself in different lighting. You look closer.
Are those the faint lines of crow’s feet? Have the “11’s” officially taken up residence between your brows? You might shrug it off. After all, wrinkles give us character. But if you’re bothered by a Perma frown or anything else, it’s nice to know you’ve got options. Antiwrinkle and filler injectables are amongst the best of them. And when done right, the results look glorious.
Join us on an information deep dive for everything you need to know to avoid uneven brows, dramatic unnatural results, and frozen faces.
What do Face injections even do to my face?
If you’ve ever wondered how cosmetic injectables wrangle wrinkles, here are the deets.
Brand X (there a few options and each clinic will have their preference) is the brand name of botulinum toxin, and it’s produced by the bacterium Clostridium botulinum. C. botulinum is found in plants, soil, water to name a few things. This chemical blocks the neurotransmitter acetylcholine, causing muscle paralysis that lasts for several months. By the muscle not moving, you will not be stretching the skin and making more lines and wrinkles in that area. It’s as simple as that!
Botulinum is a potent substance that affects the nervous system but fear not! it is completely safe when used to minimize wrinkles, as it’s administered in super small doses. It’s often used in large doses to treat some medical conditions. The muscle paralysis effect is how an antiwrinkle injection reduces the crinkling and wrinkling that naturally happens when we make certain expressions (and simply, aging). In some cases, it may even prevent further creasing.
For the sake of beauty, is it actually safe?
That all sounds a little freaky, right? We’re talking about an injection with poisonous origins, and it’s being injected into faces all over the world!
Yes! However scientific researchers consider this to be extremely safe. It is even safer when compared to other, more-invasive cosmetic procedures.
Before you get your face jabs, make sure you read up on your clinic
1. How to choose the right clinic
Face injections are currently the top nonsurgical cosmetic procedure in Australia. That means there are a lot of cosmetic clinics out there and it’s up to you to choose the right one.
First check website and social media to see if your clinic’s work matches your desired aesthetic. Think of it in much the same way you would if getting a tattoo, you’d take a good look at the artist’s portfolio, right? Do the same with a cosmetic clinic to fix your face.
Secondly, look at their previous before and after results, then read online reviews about the clinic you are planning to visit.
Once you’ve narrowed down your list, schedule a consultation to see if their philosophy aligns with yours. It’s your face, your budget, your decision, you have to choose your provider.
If you feel pressured by a provider, walk away — and fast. Finding a cosmetic clinic for your face is about finding a skilled practitioner who listens to your concerns and desires and does not push you into treatments you are not comfortable with. Your cosmetic clinic needs to be your collaborator in helping you achieve your goals, not dictate your goals to you.
Finding the right Cosmetic Clinic
Consider credentials and experience
Research the clinic’s previous work
Check online reviews
Meet the practitioner face to face for a consultation
Does their philosophy align with your goals?
2. Make a treatment plan with your Cosmetic Clinic
When you’ve settled on a clinic, make a treatment plan with them in your consultation. Remember that your face is unique and attached to a unique individual. That means that your facial treatment plan will be different than your bestie’s.
The most important part of creating any plan for your face is understanding your goals and establishing realistic expectations, and depending on your goals, you may need to visit the clinic up a few times a year for different treatments. Your face cosmetic clinic should outline all your options, including treatments not related to anti-wrinkle injections, treatments such as skin needling which are collagen stimulating treatments.
Once you share your skin and face goals, the clinic should consider your age and look closely at the depth of your facial creases. Most clinics prefer to use neurotoxin to treat fine wrinkles. For deeper set lines in the face, filler is most often used and could be used alongside additional procedures such as skin boosters to achieve a person’s desired aesthetic.
Your skin clinic should also evaluate all your dynamic muscle movements. In regard to forehead lines, for example, the clinic will see how a patient looks with eyebrows raised, at rest, and with eyes closed.
Please note, there are some people who have genetically heavy eyelids who compensate by keeping their eyebrows raised all the time, having anti-wrinkle injections to the forehead can weaken these muscles and prevent the compensatory raise. As a result, the person would feel like their lids are even heavier – not a desired aesthetic. Choose wisely and make a comsetic treatment plan.
How to create your face cosmetic plan
What are your goals?
Can your goals be achieved with antiwrinkle and filler treatments?
Consider your age
Discuss skin needling and other facial treatments
Consider your budget
Discuss lifestyle factors
Think about your lifestyle and talk to the cosmetic clinic about how it impacts your skin. Aging occurs because of both intrinsic and extrinsic factors. Our genes, ethnicity, and even certain medical conditions are intrinsic, and we don’t have control over them. We have more control over extrinsic factors, like air pollution, sun exposure, stress or smoking.
Educating the patient about the different types of aging and having a candid discussion about their particular habits, environmental exposures, as well as their diet and lifestyle choices will help you clinic guide the plan, maximize the benefits, and optimize the results.
What’s the right age to get Face Injections?
Although the time frame will be different for everyone, most medical professionals recommend antiwrinkle treatment to the face when those fine lines appear and start to bother you. You’ll know!
In our 30s, our skin cell turnover and our collagen production begins to slow down and this is generally when many of us begin to see the signs of aging. Some people might choose to get preventative facial injections before then and that does have merit. Please be aware if you are under 18 years of age you are unable to obtain treatments in most clinics in Australia.
To find out what Harbour Medispa’s facial cosmetic treatments or to book your obligation free cosmetic consultation. We are 3km out of the city in a quiet, leafy environment with easy and plentiful free parking. Contact us for an appointment.