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Is Nicotine Gum still recommended?

Discussion in 'The Cave' started by PaulG, Sep 28, 2019.

  1. PaulG

    PaulG New Member

    I have been on nicotine gum for 2yrs on and off and am physically and psychologically addicted. Pro and cons below making me realise I should quit. I am doing super high amounts because of the addiction. eg 16mg 8 times a day on average. Definetely less cons during summer when I get more UV

    • Cognitive boost
    • Dream recall
    • Energy increase - slight

    • Expensive
    • Addictive
    • Poor gut health
    • Mucous at night sometimes effecting time to sleep
    • Difficulty sleeping
    • Feeling amped and it being the norm
    I definetely experience many of the health benefits mentioned in this article


    Should I be upping levels of nicotine beneficial co-factors, maybe ascorbic acid (Vitamin-C)


    Numerous epidemiological studies have reported that tobacco smoking is a major risk factor for oral cancer, but relatively little is known about the effect of nicotine, a major product of cigarette smoking, on immortalized oral keratinocytes and cancer cells.

    We investigated the effects of nicotine on the growth and differentiation of immortalized human oral keratinocytes (IHOK), primary oral cancer cells (HN4), metastatic oral cancer cells (HN12), and human skin keratinocytes (HaCaT), in the monolayer and in the three-dimensional (3D) raft cultures using the MTT assay, Western blotting, and cell cycle analysis.

    Nicotine inhibited the proliferation of immortalized and malignant keratinocytes in dose- and time-dependent manners as determined by MTT assay. The 3D organotypic culture showed that nicotine at high concentration (300 microM) inhibits epithelial maturation, surface keratinization, and decreased epithelial thickness. Flow cytometry showed that nicotine inhibited cell cycle progression by inducing G(0)/G(1) arrest of HaCaT, IHOK, HN4, and HN12 cells without causing apoptosis. Nicotine treatment increased p21 expression in immortalized cells (HaCaT, IHOK) and oral cancer cells (HN4, HN12), but decreased pRb and p53 expression in oral cancer cells. Moreover, after high-dose nicotine treatment, the involucrin expression increased markedly in immortalized cells, but not in oral cancer cells.

    We demonstrated that nicotine inhibits growth through cell cycle arrest at G(0)/G(1) phase probably by increasing the expression of p21(WAF1/CIP1). Nicotine also affects epithelial differentiation in immortalized and malignant oral keratinocytes. Malignant oral keratinocytes appear to be more resistant to the effects of nicotine on epithelial growth and differentiation as compared to the immortalized cells.

    Pro-inflammatory cytokines are also crucial for early responses to pathogens and the up-regulation of local host defences. Several cytokines such as IL-1β, IL-10, IL-12 and TNF-α are produced by DCs in response to bacterial antigens. Our data provide evidence that DCs exposed to nicotine produce lower levels of IL-1β, IL-10, TNF-α and, most notably, IL-12 (Fig. 3). IL-12, a potent pro-inflammatory cytokine, plays a central role in the initiation and control of cell-mediated immunity.24,38,39 Importantly, IL-12 produced by DCs during early antigenic stimulation has been reported to be a powerful inducer of Th1 responses, and defects in its production have been suggested to be a factor contributing to immune depression.4042 Hence, the direct effect on DC cytokine production, particularly that of IL-12, may suggest another mechanism by which nicotine affects host defences against infection and cancer.

    It is well established that DCs are APC specialized for naïve T-cell activation in vitro and in vivo.16,17,31 T cells from smokers have shown a decreased ability to proliferate in response to T-cell mitogens.9 Our data revealed a reduction in T-cell proliferation induced by DCs in the nicotinic environment (Fig. 4a), which was supported by the decreased number of activated CD4 and CD8 T cells (Fig. 7). However, the T-cell hyporesponsiveness seen in our assays was not a result of T-cell anergy. Indeed, T cells co-cultured with DCs in the presence of nicotine produced equal amounts of IL-2 (Fig. 5) compared with control T cells. Moreover, the addition of exogenous IL-2 did not reverse this stage of hyporesponsiveness (data not shown). Finally, we did not observe any changes in the viability of T cells obtained from co-cultures, suggesting that the functional inactivation of T cells was the result of a non-deletional mechanism mediated by nicotine. Interestingly, nicotine did not inhibit APC-independent T-cell proliferation induced by anti-CD3/CD28 Abs (Fig. 4b), confirming no direct effect of nicotine on T-cell responses.

    From our data, it appears that nicotine has some inhibitory effect on both APC-dependent and -independent IFN-γ production by primary T cells (Fig. 5). Whereas T cells stimulated with anti-CD3/CD28 Abs were able to produce similar amounts of IFN-γ once re-stimulated in the absence of nicotine, T cells stimulated with DCs produced significantly lower levels of IFN-γ upon re-stimulation (Fig. 6). Importantly, these results were correlated with a reduction in the frequency of IFN-γ-producing T cells when DCs were used as stimulators (Fig. 8). These data indicate that nicotine had a direct effect on the ability of DCs to polarize Th1 cells. Interestingly, supplementation of IL-12 alone in the primary co-cultures could not restore DC capacity to the control level (data not shown). We surmised that, during DC/T-cell interaction, nicotine may affect the expression of accessory molecules on DCs that are critical for T-cell responsiveness to IL-12 and final Th1 polarization. Indeed, we found that, in a nicotinic environment, fully matured irradiated DCs were able to provide the necessary signals for expansion of IFN-γ-producing T cells (Fig. 8). Considering the data outlined above, it is reasonable to conclude that, prior to or upon DC/T-cell interaction, nicotine specifically impairs DC immunostimulatory functions through its effects on DC antigen capture/presentation and IL-12 shortening, and other possible mechanisms.

    The concentration of nicotine in local tissue (i.e. the respiratory tract), where tissue-resident DCs encounter antigens, may be higher than the level of nicotine reported in the plasma of heavy smokers.43 It is estimated that daily nicotine intake and intake per cigarette from nominal brands smoked are 18·6 and 1·28 mg, respectively.44 It has also been stated that the average cigarette contains approximately 10 mg of nicotine,45 and between 1 and 2 mg of nicotine is delivered to the lungs when a cigarette is smoked.46 In addition, Russell et al.47 reported that the salivary concentration of nicotine reaches 1560 µg/ml in smokeless-tobacco users. From these studies, one may infer that, after a cigarette has been smoked, the concentration of nicotine in the local tissue reaches the level used in this work and hence that this is physiologically relevant.

    The present work provides new information on the immunosuppressive effect of nicotine on the DC system and adds to our understanding of the ways in which exposure to cigarette smoke may increase the risks of infection and cancer.

    I do worry about my mitichondria and my gut health
  2. Phosphene

    Phosphene Gold (finally)

    Curious about this too. I’m not a smoker and haven’t tried the gum yet. Been in too good a mood naturally this summer to even consider it, but might keep it in my arsenal for the winter.

    Or maybe I’ll try methylene blue first, assuming that’s still recommended too?
  3. MITpowered26

    MITpowered26 New Member

    SWIM - someone other than me.


    I hesitate to chime in. I don’t know much about nicotine with respect to mitochondria. But I do have some sense, as a pharmacist, giving you ideas how to get off that’s stuff. A couple questions though:

    1. Did this habit start from smoking initially?

    2. Is there ever a moment during the yearly cycle, where you consume zero nicotine gum. If not, what is the minimum u tend to consume?
  4. MITpowered26

    MITpowered26 New Member

    Swim should preface:

    The above is assuming

    A. You want to quit

    B. You need to quit

    The end long-term game, I sense, is that light Water and magnetism should heal your mitochondria and you eventually shouldn’t need nicotine...
    PaulG likes this.
  5. PaulG

    PaulG New Member

    Yes I tend to go 2 weeks on, 1 week off. I think I can get off it and have tried quite a few times. I dont think I will have any problems coming off from a withdrawal point of view. I will quit it this week.
  6. MITpowered26

    MITpowered26 New Member

    Keep us posted.
  7. MITpowered26

    MITpowered26 New Member

    Swim thought about this some more and just wanted to add one More thing out of duty to tell you the truth and not to harm you:

    Withdrawal is not just negative effects of quitting.. it is the lack of positive effects ... eg . “Cognitive boost.” Feeling like you are psychological and physiological “addicted” to nicotine clues me in that you are struggling to quit with lasting impact due to a withdrawal from “lack of effect”.
    PaulG and Phosphene like this.
  8. MITpowered26

    MITpowered26 New Member

    Swim adds:

    This may sound like fluff: but the strategies for a taper plan don’t differ much between “side effect” withdrawal” and “lack of effect” withdrawal. That’s the point swim is trying to make.
    Phosphene likes this.
  9. Lahelada

    Lahelada New Member

  10. Bonnie

    Bonnie Gold

    I certainly get a cognitive boost. I usually do one half of 1 mg Nicorette and have the other half in the afternoon. What is everyone else finding?
  11. Jack Kruse

    Jack Kruse Administrator

    I answered it on Q and A last night for someone

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